Esv2n49
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1. The document discusses the potential role of heat shock protein 65 (HSP-65) as an autoantigen in the development of atherosclerotic plaques. Several studies have found associations between antibodies to HSP-65 and various measures of atherosclerosis. 2. One study immunized rabbits with the BCG vaccine, which contains HSP-65, and found higher levels of atherosclerotic plaques in immunized rabbits compared to controls. This suggests HSP-65 immunity may enhance atherosclerosis. 3. However, the role of HSP-65 is unclear - it may be more important for plaque vulnerability rather than generation, and different antigens could be involved at different stages or between patients.
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Aeha immune mechanisms in atherosclerosis
This document summarizes the role of the immune system in atherosclerosis. It finds that:
1) Adaptive immunity plays a major role in atherosclerosis as mice lacking T and B cells develop dramatically less atherosclerosis despite similar cholesterol levels.
2) T cells in lesions recognize oxidized LDL and other antigens, activating macrophages and promoting inflammation.
3) NKT cells increase atherosclerosis by recognizing glycolipid antigens, while regulatory T cells and B cells decrease disease by producing anti-inflammatory cytokines like IL-10 and TGF-β.
4) Protective immunization approaches have shown promise in animal models by stimulating antibody production against oxidized LDL and other antigens to decrease plaque formation.
Atherosclerosis, an autoimmune disease
1. Autoimmune reactions against heat shock proteins (HSPs), particularly HSP60, may play an important role in the early development of atherosclerosis.
2. HSPs released from necrotic cells in advanced atherosclerotic plaques can stimulate the innate immune response and promote inflammation, attracting more inflammatory cells. This may link HSPs to complications like plaque rupture or thrombosis.
3. Both humoral and cellular immune reactions against HSP60 work together with classical cardiovascular risk factors to promote atherosclerosis and its complications.
Atherosclerosis an autoimmune disease
1. Autoimmune reactions against heat shock proteins (HSPs), particularly HSP60, may play an important role in the early development of atherosclerosis by attracting immune cells into the arterial wall.
2. HSPs released from dying cells in advanced atherosclerotic plaques can stimulate the innate immune response and promote inflammation, attracting more immune cells and linking to complications like plaque rupture.
3. Both humoral and cellular immune responses against HSP60 work together with classical risk factors to develop and progress atherosclerosis.
Atherosclerosis, an autoimmune disease 2
1. Autoimmune reactions against heat shock proteins (HSPs), particularly HSP60, may play an important role in the early development of atherosclerosis.
2. HSPs released from necrotic cells in advanced atherosclerotic plaques can stimulate the innate immune response and promote inflammation, attracting more inflammatory cells. This may link HSPs to complications like plaque rupture and thrombosis.
3. Both humoral and cellular immune reactions against HSP60 work together with classical risk factors to promote atherosclerosis and its progression.
Autoimmune disease
1. Autoimmune reactions against heat shock proteins (HSPs), particularly HSP60, may play an important role in the early development of atherosclerosis.
2. HSPs released from necrotic cells in advanced atherosclerotic plaques can stimulate the innate immune response and promote inflammation, attracting more inflammatory cells. This may link HSPs to complications like plaque rupture or thrombosis.
3. Both humoral and cellular immune reactions against HSP60 work together with classical cardiovascular risk factors to promote atherosclerosis and its complications.
243 b cell
I. The document summarizes several studies that investigated the role of the immune system, particularly B cells, in atherosclerosis using mouse models.
II. One study found that RAG-1 deficient mice, which lack functional B and T cells, exhibited increased neointimal formation following arterial injury compared to wild type mice. Transferring B cells from wild type mice to RAG-1 deficient mice reduced neointimal formation.
III. Overall, the studies suggest that B cells may play a protective role against atherosclerosis by reducing plaque formation and progression. The mechanism may involve antibodies that target oxidation-specific epitopes, but this requires further investigation.
Esv2n15
I. The document summarizes several studies that investigated the role of the immune system, particularly B cells, in atherosclerosis using mouse models.
II. One study found that RAG-1 deficient mice, which lack functional B and T cells, exhibited increased neointimal formation following arterial injury compared to wild type mice. Transferring B cells from wild type mice to RAG-1 deficient mice reduced neointimal formation.
III. Overall, the studies suggest that B cells may play a protective role against atherosclerosis by reducing plaque formation and progression. The mechanism may involve antibodies that target oxidation-specific epitopes, but this requires further investigation.
Towards immune modulation vp
This document discusses potential immune-based therapies for modulating atherosclerosis and vulnerable plaque. It suggests that targeting specific antigens, co-stimulatory molecules, cytokines, vaccines, recombinant proteins, antibodies, cells, or small molecule drugs could help shift the immune response away from pathogenic Th1 immunity toward protective Th2 immunity. Certain cytokines like IL-10 and TGFβ may be protective, while IFNγ and TNFα aggravate disease. Immunization experiments with oxidized LDL and heat shock protein 65 have shown promise in reducing lesions in animal models. Statins and pentoxifyllin may also help by inhibiting Th1 responses. However, general immunosuppression poses side effects, so focused immune modulation is a more viable strategy
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Aeha immune mechanisms in atherosclerosis
This document summarizes the role of the immune system in atherosclerosis. It finds that:
1) Adaptive immunity plays a major role in atherosclerosis as mice lacking T and B cells develop dramatically less atherosclerosis despite similar cholesterol levels.
2) T cells in lesions recognize oxidized LDL and other antigens, activating macrophages and promoting inflammation.
3) NKT cells increase atherosclerosis by recognizing glycolipid antigens, while regulatory T cells and B cells decrease disease by producing anti-inflammatory cytokines like IL-10 and TGF-β.
4) Protective immunization approaches have shown promise in animal models by stimulating antibody production against oxidized LDL and other antigens to decrease plaque formation.
Atherosclerosis, an autoimmune disease
1. Autoimmune reactions against heat shock proteins (HSPs), particularly HSP60, may play an important role in the early development of atherosclerosis.
2. HSPs released from necrotic cells in advanced atherosclerotic plaques can stimulate the innate immune response and promote inflammation, attracting more inflammatory cells. This may link HSPs to complications like plaque rupture or thrombosis.
3. Both humoral and cellular immune reactions against HSP60 work together with classical cardiovascular risk factors to promote atherosclerosis and its complications.
Atherosclerosis an autoimmune disease
1. Autoimmune reactions against heat shock proteins (HSPs), particularly HSP60, may play an important role in the early development of atherosclerosis by attracting immune cells into the arterial wall.
2. HSPs released from dying cells in advanced atherosclerotic plaques can stimulate the innate immune response and promote inflammation, attracting more immune cells and linking to complications like plaque rupture.
3. Both humoral and cellular immune responses against HSP60 work together with classical risk factors to develop and progress atherosclerosis.
Atherosclerosis, an autoimmune disease 2
1. Autoimmune reactions against heat shock proteins (HSPs), particularly HSP60, may play an important role in the early development of atherosclerosis.
2. HSPs released from necrotic cells in advanced atherosclerotic plaques can stimulate the innate immune response and promote inflammation, attracting more inflammatory cells. This may link HSPs to complications like plaque rupture and thrombosis.
3. Both humoral and cellular immune reactions against HSP60 work together with classical risk factors to promote atherosclerosis and its progression.
Autoimmune disease
1. Autoimmune reactions against heat shock proteins (HSPs), particularly HSP60, may play an important role in the early development of atherosclerosis.
2. HSPs released from necrotic cells in advanced atherosclerotic plaques can stimulate the innate immune response and promote inflammation, attracting more inflammatory cells. This may link HSPs to complications like plaque rupture or thrombosis.
3. Both humoral and cellular immune reactions against HSP60 work together with classical cardiovascular risk factors to promote atherosclerosis and its complications.
243 b cell
I. The document summarizes several studies that investigated the role of the immune system, particularly B cells, in atherosclerosis using mouse models.
II. One study found that RAG-1 deficient mice, which lack functional B and T cells, exhibited increased neointimal formation following arterial injury compared to wild type mice. Transferring B cells from wild type mice to RAG-1 deficient mice reduced neointimal formation.
III. Overall, the studies suggest that B cells may play a protective role against atherosclerosis by reducing plaque formation and progression. The mechanism may involve antibodies that target oxidation-specific epitopes, but this requires further investigation.
Esv2n15
I. The document summarizes several studies that investigated the role of the immune system, particularly B cells, in atherosclerosis using mouse models.
II. One study found that RAG-1 deficient mice, which lack functional B and T cells, exhibited increased neointimal formation following arterial injury compared to wild type mice. Transferring B cells from wild type mice to RAG-1 deficient mice reduced neointimal formation.
III. Overall, the studies suggest that B cells may play a protective role against atherosclerosis by reducing plaque formation and progression. The mechanism may involve antibodies that target oxidation-specific epitopes, but this requires further investigation.
Towards immune modulation vp
This document discusses potential immune-based therapies for modulating atherosclerosis and vulnerable plaque. It suggests that targeting specific antigens, co-stimulatory molecules, cytokines, vaccines, recombinant proteins, antibodies, cells, or small molecule drugs could help shift the immune response away from pathogenic Th1 immunity toward protective Th2 immunity. Certain cytokines like IL-10 and TGFβ may be protective, while IFNγ and TNFα aggravate disease. Immunization experiments with oxidized LDL and heat shock protein 65 have shown promise in reducing lesions in animal models. Statins and pentoxifyllin may also help by inhibiting Th1 responses. However, general immunosuppression poses side effects, so focused immune modulation is a more viable strategy
075 immune modulation
This document discusses potential immune-based therapies for modulating atherosclerosis and vulnerable plaque. It summarizes that:
1. Specific antigens, co-stimulatory molecules, cytokines, vaccines, recombinant proteins, antibodies, and cells could be potential targets for immunomodulation of atherosclerosis.
2. While general immunosuppression may reduce atherosclerosis in animal studies, it has substantial side effects for infections and direct vascular effects that make it unsuitable for chronic treatment in humans.
3. Modulating the Th1/Th2 balance, inducing protective antibodies through vaccination against oxidized LDL or heat shock proteins, and using small molecule drugs that inhibit Th1 responses like statins and pentoxifyllin are promising
Towards immune modulation vp 16 11 gkh
This document discusses potential immune-based therapies for modulating atherosclerosis and vulnerable plaque. It suggests that targeting specific antigens, co-stimulatory molecules, cytokines, vaccines, recombinant proteins, antibodies, cells, or small molecule drugs could help shift the immune response away from pathogenic Th1 immunity toward protective Th2 immunity. Several approaches show promise, such as immunizing against oxidized LDL to induce atheroprotective antibodies, administering heat shock protein 65 to reduce lesions, or using drugs like statins or pentoxifyllin that can inhibit Th1 responses and atherosclerosis in animal models. However, challenges remain as general immunosuppression could increase infection risk while cytokines may have undesirable side effects.
501 autoimmune disease
1. Autoimmune reactions against heat shock proteins (HSPs), particularly HSP60, may play an important role in the early development of atherosclerosis.
2. HSPs released from necrotic cells in advanced atherosclerotic plaques can stimulate the innate immune response and promote inflammation, attracting more inflammatory cells. This may link HSPs to complications like plaque rupture and thrombosis.
3. Both humoral and cellular immune reactions against HSP60 work together with classical cardiovascular risk factors to promote atherosclerosis and its complications.
Atherosclerosis an autoimmune disease
1. Autoimmune reactions against heat shock proteins (HSPs), particularly HSP60, may play an important role in the early development of atherosclerosis.
2. HSPs released from necrotic cells in advanced atherosclerotic plaques can stimulate the innate immune response and promote inflammation, attracting more inflammatory cells and linking to complications like plaque rupture or thrombosis.
3. Both humoral and cellular immune reactions against HSP60 work together with classical risk factors to develop and progress atherosclerosis.
Drnaghavi
1) Influenza infection was found to exert prominent inflammatory and thrombotic effects on atherosclerotic plaques in aged Apo E-deficient mice.
2) About one third of the infected mice showed striking intimal infiltrates in the aorta and most of these mice died or were sacrificed between days 4-10 post infection.
3) Administration of cytokines mimicking influenza infection resulted in greater iron accumulation in macrophage-rich regions of plaques compared to controls, indicating enhanced macrophage homing to plaques.
Hyper Ig M Syndrome
This document outlines the molecular basis and clinical manifestations of different types of hyper-IgM syndrome. It discusses 6 types of HIGM defined by genetic defects such as CD40L, AICDA, CD40, and UNG deficiencies. The clinical features include recurrent infections, enlarged lymph nodes, impaired class switch recombination, and variable defects in somatic hypermutation. Diagnosis involves assessing serum immunoglobulin levels and identifying genetic mutations associated with each type.
074 influenza infection effects
1) Influenza infection exerts prominent inflammatory and thrombotic effects on atherosclerotic plaques in aged Apo E-deficient mice. Approximately one third of the mice showed increased plaque inflammation and some died 4-10 days after influenza inoculation.
2) A protocol was tested using cytokines and SPIO nanoparticles to enhance macrophage homing to plaques in Apo E-deficient mice. Mice that received cytokines prior to SPIO injection showed more iron-labeled macrophages in plaques compared to controls.
3) The results suggest that influenza infection exacerbates plaque inflammation in mice and cytokines may account for some of the effects of influenza on atherosclerosis. Longer studies are needed to determine if plaque
Designer Antibodies
Designer antibodies that bind to both CD3 receptors on T-cells and HIV proteins on infected cells have shown promise in laboratory experiments as a potential approach to eliminating HIV reservoirs and achieving a cure. These bispecific antibodies act to bridge infected cells and T-cells, activating latent virus and marking the infected cells for destruction. While early studies in mice were problematic, more recent studies using improved antibody designs have activated and lysed latent HIV-infected human cells in test tubes without significant safety issues. However, successfully translating this approach to safe and effective human trials faces challenges including fully understanding and targeting all HIV reservoir sites and gaining acceptance within HIV/AIDS communities.
Influenza infection exerts prominent
1) Influenza infection causes prominent inflammatory and thrombotic effects on atherosclerotic plaques in aged Apo E-deficient mice.
2) About one third of infected mice showed striking intimal plaque infiltrates and most of these mice died within 10 days.
3) Administration of cytokines like TNF-α, IL-1β, and IFN-γ to mimic influenza infection enhanced iron accumulation in macrophage-rich plaques, indicating increased macrophage homing to plaques.
Hyper IgM Syndrome
Hyper IgM Syndrome, also known as X-linked immunodeficiency with hyper–immunoglobulin M, is caused by mutations in the CD40 ligand gene which is required for immunoglobulin class switching. This leads to elevated IgM levels but reduced IgG, IgA, and IgE. Patients have recurrent infections, pneumonia being most common, and are at risk for autoimmune disorders. Physical exam may reveal oral ulcers, lymphadenopathy, or hepatosplenomegaly related to infection. Differential diagnoses include common variable immunodeficiency, severe combined immunodeficiency, and agammaglobulinemia.
Transplant rejection and GVD
1. Transplant rejection occurs when the recipient's immune system attacks the transplanted organ or graft, recognizing it as foreign. It can involve cell-mediated immunity or circulating antibodies.
2. Graft versus host disease occurs when immune cells from the donor engraft in the recipient and attack the recipient's body, seeing it as foreign. It is a risk for allogenic stem cell or solid organ transplants from a donor.
3. Treatment for rejection and GVHD involves immunosuppressive drugs like steroids, ATG, mycophenolate, and antibodies targeting immune cells and cytokines.
Ss1
This document lists over 60 potential factors that are known to cause false positive HIV antibody test results. These factors include naturally occurring antibodies, viral infections like hepatitis B, autoimmune diseases, organ transplants, blood transfusions, and various medical treatments. False positives can also be caused by cross-reactivity with antibodies against other viruses or proteins as well as certain laboratory testing issues. Proper screening and confirmatory testing is necessary to avoid incorrect HIV diagnoses due to false positive initial test results from these many different sources.
Ebv paper mult scler 2014-pender-1352458514521888
This document describes a case study of a patient with secondary progressive multiple sclerosis who was treated with adoptive immunotherapy using Epstein-Barr virus (EBV)-specific CD8+ T cells. The treatment involved expanding the patient's autologous EBV-specific T cells in vitro and then infusing them back into the patient. The treatment was well tolerated with no significant adverse effects. Following treatment, the patient showed clinical improvements in symptoms along with reductions in disease activity on MRI scans and intrathecal immunoglobulin production, providing proof-of-principle that EBV-specific adoptive immunotherapy may be a safe and effective treatment for multiple sclerosis.
bongha shin transplantation paper
1) The study examined the effects of various immunosuppressive drugs on antibody-mediated natural killer (NK) cell activation in vitro.
2) Cyclosporine A and tacrolimus significantly reduced interferon-gamma production by NK cells in a dose-dependent manner but had a minimal effect on degranulation. Prednisone significantly reduced both interferon-gamma production and degranulation by NK cells.
3) Combining calcineurin inhibitors with prednisone additively suppressed interferon-gamma production and degranulation by NK cells activated via antibody-dependent cellular cytotoxicity, suggesting these drugs may help reduce antibody-mediated rejection after transplantation.
Esv2n33
Toll-like receptor 4 (TLR4) activation has been linked to atherosclerosis through several pathways. Mouse models show that TLR4 deficiency reduces atherosclerotic plaque formation. TLR4 is expressed in arterial wall cells like endothelial cells, smooth muscle cells, and adventitial fibroblasts. Activation of adventitial fibroblast TLR4 by factors like lipopolysaccharide can stimulate neointima formation and plaque development possibly through increased migration and proliferation of smooth muscle cells. Both luminal and adventitial TLR4 activation may contribute to atherosclerosis through inducing inflammatory cytokines and chemokines, cell migration, and matrix turnover.
Adventitial fat presentation
1) The study investigated the uptake of SPIO (superparamagnetic iron oxide), an MRI contrast agent, by periadventitial fat in an atherosclerosis mouse model.
2) Results showed significantly greater uptake of iron in the periadventitial fat of apoE k/o mice compared to control mice, as measured by iron particles and area.
3) Preliminary evidence also suggests uptake of iron in the periadventitial fat of atherosclerotic rabbits and humans, suggesting macrophage-like activity in this tissue that warrants further investigation into its role in atherosclerosis and potential applications for plaque imaging.
Falk
The document defines plaque rupture as the structural failure of the fibrocellular cap separating an atheromatous core from the lumen of an atherosclerotic artery, not just missing endothelium. It then discusses various risk factors for plaque rupture like lipid-rich core, inflammation, infection, homocysteine levels, and coronary calcium. Several studies are summarized that show plaque rupture is the cause of fatal thrombosis in 75-100% of cases of acute MI or sudden cardiac death when examined at autopsy or medical exam. The risk is similar between Europe, Asia, and the US. Plaque rupture is more common than erosion in those over age 60 and in men.
Figuresforpaper 3
This document introduces a hypothesis that spatial heterogeneity within plaques may provide information about regional mechanisms independent of classical risk factors. It aims to use a new 3D histology technique to provide evidence that local accumulation of lipids activates inflammatory cells to produce plaque-weakening factors. Graphs show measurements of plaque area, macrophage density, lipid density, smooth muscle cell density, and a vulnerability index at different distances from the renal artery.
Herrera
The document discusses the potential of the Tg53 rat model for modeling human coronary artery disease and vulnerable plaques. The model exhibits several promising features, including plaque development specifically in the coronary arteries similar to humans. Plaques in the model progress through stages and demonstrate features resembling vulnerable human plaques. The model also offers advantages as an experimental system like a defined genetic background and ability to manipulate factors like diet. Overall, the Tg53 rat model shows potential for gaining new insights into plaque development and testing novel prevention strategies, though no single model can perfectly capture the human condition.
Esv2n32
- A study examined ruptured coronary plaques in patients with acute coronary syndrome using intravascular ultrasound (IVUS) and found ruptured plaques not just at the culprit lesion but also in other vessels.
- Both culprit lesions and additional ruptured plaques showed positive arterial remodeling, where the vessel expands to accommodate plaque growth.
- Positive remodeling is associated with plaque vulnerability and unstable coronary syndromes, while negative remodeling is more common in stable lesions and involves vessel constriction around plaque.
- The direction of remodeling may represent different inflammatory stages of plaque development, with positive remodeling indicating early active lesions and negative remodeling indicating more stabilized advanced lesions.
125 ct based characterization
Growing evidence suggests that CT-based characterization of coronary plaques and arteries is possible. 16 slice multi-detector CT allows reliable detection of coronary obstructions when combined with heart rate control. It can also identify soft, intermediate, and calcified plaques. This technology has great potential as an initial non-invasive technique to identify vulnerable plaque in at-risk patients. The combination of CT imaging and serum markers may provide a powerful predictive tool for assessing vulnerability.
233 cd40
CD40 and its ligand CD40L play an important role in atherosclerosis by promoting inflammation. Statins can limit the expression of CD40 and CD40L, thereby reducing inflammation. Oxidized LDL increases the expression of CD40 and CD40L on endothelial cells, smooth muscle cells, and macrophages, further promoting atherosclerosis. CD40L also contributes to thrombosis and restenosis. While CD40 does not seem to affect early plaque formation, its deficiency is associated with more stable plaques at advanced stages of atherosclerosis.
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075 immune modulation
This document discusses potential immune-based therapies for modulating atherosclerosis and vulnerable plaque. It summarizes that:
1. Specific antigens, co-stimulatory molecules, cytokines, vaccines, recombinant proteins, antibodies, and cells could be potential targets for immunomodulation of atherosclerosis.
2. While general immunosuppression may reduce atherosclerosis in animal studies, it has substantial side effects for infections and direct vascular effects that make it unsuitable for chronic treatment in humans.
3. Modulating the Th1/Th2 balance, inducing protective antibodies through vaccination against oxidized LDL or heat shock proteins, and using small molecule drugs that inhibit Th1 responses like statins and pentoxifyllin are promising
Towards immune modulation vp 16 11 gkh
This document discusses potential immune-based therapies for modulating atherosclerosis and vulnerable plaque. It suggests that targeting specific antigens, co-stimulatory molecules, cytokines, vaccines, recombinant proteins, antibodies, cells, or small molecule drugs could help shift the immune response away from pathogenic Th1 immunity toward protective Th2 immunity. Several approaches show promise, such as immunizing against oxidized LDL to induce atheroprotective antibodies, administering heat shock protein 65 to reduce lesions, or using drugs like statins or pentoxifyllin that can inhibit Th1 responses and atherosclerosis in animal models. However, challenges remain as general immunosuppression could increase infection risk while cytokines may have undesirable side effects.
501 autoimmune disease
1. Autoimmune reactions against heat shock proteins (HSPs), particularly HSP60, may play an important role in the early development of atherosclerosis.
2. HSPs released from necrotic cells in advanced atherosclerotic plaques can stimulate the innate immune response and promote inflammation, attracting more inflammatory cells. This may link HSPs to complications like plaque rupture and thrombosis.
3. Both humoral and cellular immune reactions against HSP60 work together with classical cardiovascular risk factors to promote atherosclerosis and its complications.
Atherosclerosis an autoimmune disease
1. Autoimmune reactions against heat shock proteins (HSPs), particularly HSP60, may play an important role in the early development of atherosclerosis.
2. HSPs released from necrotic cells in advanced atherosclerotic plaques can stimulate the innate immune response and promote inflammation, attracting more inflammatory cells and linking to complications like plaque rupture or thrombosis.
3. Both humoral and cellular immune reactions against HSP60 work together with classical risk factors to develop and progress atherosclerosis.
Drnaghavi
1) Influenza infection was found to exert prominent inflammatory and thrombotic effects on atherosclerotic plaques in aged Apo E-deficient mice.
2) About one third of the infected mice showed striking intimal infiltrates in the aorta and most of these mice died or were sacrificed between days 4-10 post infection.
3) Administration of cytokines mimicking influenza infection resulted in greater iron accumulation in macrophage-rich regions of plaques compared to controls, indicating enhanced macrophage homing to plaques.
Hyper Ig M Syndrome
This document outlines the molecular basis and clinical manifestations of different types of hyper-IgM syndrome. It discusses 6 types of HIGM defined by genetic defects such as CD40L, AICDA, CD40, and UNG deficiencies. The clinical features include recurrent infections, enlarged lymph nodes, impaired class switch recombination, and variable defects in somatic hypermutation. Diagnosis involves assessing serum immunoglobulin levels and identifying genetic mutations associated with each type.
074 influenza infection effects
1) Influenza infection exerts prominent inflammatory and thrombotic effects on atherosclerotic plaques in aged Apo E-deficient mice. Approximately one third of the mice showed increased plaque inflammation and some died 4-10 days after influenza inoculation.
2) A protocol was tested using cytokines and SPIO nanoparticles to enhance macrophage homing to plaques in Apo E-deficient mice. Mice that received cytokines prior to SPIO injection showed more iron-labeled macrophages in plaques compared to controls.
3) The results suggest that influenza infection exacerbates plaque inflammation in mice and cytokines may account for some of the effects of influenza on atherosclerosis. Longer studies are needed to determine if plaque
Designer Antibodies
Designer antibodies that bind to both CD3 receptors on T-cells and HIV proteins on infected cells have shown promise in laboratory experiments as a potential approach to eliminating HIV reservoirs and achieving a cure. These bispecific antibodies act to bridge infected cells and T-cells, activating latent virus and marking the infected cells for destruction. While early studies in mice were problematic, more recent studies using improved antibody designs have activated and lysed latent HIV-infected human cells in test tubes without significant safety issues. However, successfully translating this approach to safe and effective human trials faces challenges including fully understanding and targeting all HIV reservoir sites and gaining acceptance within HIV/AIDS communities.
Influenza infection exerts prominent
1) Influenza infection causes prominent inflammatory and thrombotic effects on atherosclerotic plaques in aged Apo E-deficient mice.
2) About one third of infected mice showed striking intimal plaque infiltrates and most of these mice died within 10 days.
3) Administration of cytokines like TNF-α, IL-1β, and IFN-γ to mimic influenza infection enhanced iron accumulation in macrophage-rich plaques, indicating increased macrophage homing to plaques.
Hyper IgM Syndrome
Hyper IgM Syndrome, also known as X-linked immunodeficiency with hyper–immunoglobulin M, is caused by mutations in the CD40 ligand gene which is required for immunoglobulin class switching. This leads to elevated IgM levels but reduced IgG, IgA, and IgE. Patients have recurrent infections, pneumonia being most common, and are at risk for autoimmune disorders. Physical exam may reveal oral ulcers, lymphadenopathy, or hepatosplenomegaly related to infection. Differential diagnoses include common variable immunodeficiency, severe combined immunodeficiency, and agammaglobulinemia.
Transplant rejection and GVD
1. Transplant rejection occurs when the recipient's immune system attacks the transplanted organ or graft, recognizing it as foreign. It can involve cell-mediated immunity or circulating antibodies.
2. Graft versus host disease occurs when immune cells from the donor engraft in the recipient and attack the recipient's body, seeing it as foreign. It is a risk for allogenic stem cell or solid organ transplants from a donor.
3. Treatment for rejection and GVHD involves immunosuppressive drugs like steroids, ATG, mycophenolate, and antibodies targeting immune cells and cytokines.
Ss1
This document lists over 60 potential factors that are known to cause false positive HIV antibody test results. These factors include naturally occurring antibodies, viral infections like hepatitis B, autoimmune diseases, organ transplants, blood transfusions, and various medical treatments. False positives can also be caused by cross-reactivity with antibodies against other viruses or proteins as well as certain laboratory testing issues. Proper screening and confirmatory testing is necessary to avoid incorrect HIV diagnoses due to false positive initial test results from these many different sources.
Ebv paper mult scler 2014-pender-1352458514521888
This document describes a case study of a patient with secondary progressive multiple sclerosis who was treated with adoptive immunotherapy using Epstein-Barr virus (EBV)-specific CD8+ T cells. The treatment involved expanding the patient's autologous EBV-specific T cells in vitro and then infusing them back into the patient. The treatment was well tolerated with no significant adverse effects. Following treatment, the patient showed clinical improvements in symptoms along with reductions in disease activity on MRI scans and intrathecal immunoglobulin production, providing proof-of-principle that EBV-specific adoptive immunotherapy may be a safe and effective treatment for multiple sclerosis.
bongha shin transplantation paper
1) The study examined the effects of various immunosuppressive drugs on antibody-mediated natural killer (NK) cell activation in vitro.
2) Cyclosporine A and tacrolimus significantly reduced interferon-gamma production by NK cells in a dose-dependent manner but had a minimal effect on degranulation. Prednisone significantly reduced both interferon-gamma production and degranulation by NK cells.
3) Combining calcineurin inhibitors with prednisone additively suppressed interferon-gamma production and degranulation by NK cells activated via antibody-dependent cellular cytotoxicity, suggesting these drugs may help reduce antibody-mediated rejection after transplantation.
Esv2n33
Toll-like receptor 4 (TLR4) activation has been linked to atherosclerosis through several pathways. Mouse models show that TLR4 deficiency reduces atherosclerotic plaque formation. TLR4 is expressed in arterial wall cells like endothelial cells, smooth muscle cells, and adventitial fibroblasts. Activation of adventitial fibroblast TLR4 by factors like lipopolysaccharide can stimulate neointima formation and plaque development possibly through increased migration and proliferation of smooth muscle cells. Both luminal and adventitial TLR4 activation may contribute to atherosclerosis through inducing inflammatory cytokines and chemokines, cell migration, and matrix turnover.
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Adventitial fat presentation
1) The study investigated the uptake of SPIO (superparamagnetic iron oxide), an MRI contrast agent, by periadventitial fat in an atherosclerosis mouse model.
2) Results showed significantly greater uptake of iron in the periadventitial fat of apoE k/o mice compared to control mice, as measured by iron particles and area.
3) Preliminary evidence also suggests uptake of iron in the periadventitial fat of atherosclerotic rabbits and humans, suggesting macrophage-like activity in this tissue that warrants further investigation into its role in atherosclerosis and potential applications for plaque imaging.
Falk
The document defines plaque rupture as the structural failure of the fibrocellular cap separating an atheromatous core from the lumen of an atherosclerotic artery, not just missing endothelium. It then discusses various risk factors for plaque rupture like lipid-rich core, inflammation, infection, homocysteine levels, and coronary calcium. Several studies are summarized that show plaque rupture is the cause of fatal thrombosis in 75-100% of cases of acute MI or sudden cardiac death when examined at autopsy or medical exam. The risk is similar between Europe, Asia, and the US. Plaque rupture is more common than erosion in those over age 60 and in men.
Figuresforpaper 3
This document introduces a hypothesis that spatial heterogeneity within plaques may provide information about regional mechanisms independent of classical risk factors. It aims to use a new 3D histology technique to provide evidence that local accumulation of lipids activates inflammatory cells to produce plaque-weakening factors. Graphs show measurements of plaque area, macrophage density, lipid density, smooth muscle cell density, and a vulnerability index at different distances from the renal artery.
Herrera
The document discusses the potential of the Tg53 rat model for modeling human coronary artery disease and vulnerable plaques. The model exhibits several promising features, including plaque development specifically in the coronary arteries similar to humans. Plaques in the model progress through stages and demonstrate features resembling vulnerable human plaques. The model also offers advantages as an experimental system like a defined genetic background and ability to manipulate factors like diet. Overall, the Tg53 rat model shows potential for gaining new insights into plaque development and testing novel prevention strategies, though no single model can perfectly capture the human condition.
Esv2n32
- A study examined ruptured coronary plaques in patients with acute coronary syndrome using intravascular ultrasound (IVUS) and found ruptured plaques not just at the culprit lesion but also in other vessels.
- Both culprit lesions and additional ruptured plaques showed positive arterial remodeling, where the vessel expands to accommodate plaque growth.
- Positive remodeling is associated with plaque vulnerability and unstable coronary syndromes, while negative remodeling is more common in stable lesions and involves vessel constriction around plaque.
- The direction of remodeling may represent different inflammatory stages of plaque development, with positive remodeling indicating early active lesions and negative remodeling indicating more stabilized advanced lesions.
125 ct based characterization
Growing evidence suggests that CT-based characterization of coronary plaques and arteries is possible. 16 slice multi-detector CT allows reliable detection of coronary obstructions when combined with heart rate control. It can also identify soft, intermediate, and calcified plaques. This technology has great potential as an initial non-invasive technique to identify vulnerable plaque in at-risk patients. The combination of CT imaging and serum markers may provide a powerful predictive tool for assessing vulnerability.
233 cd40
CD40 and its ligand CD40L play an important role in atherosclerosis by promoting inflammation. Statins can limit the expression of CD40 and CD40L, thereby reducing inflammation. Oxidized LDL increases the expression of CD40 and CD40L on endothelial cells, smooth muscle cells, and macrophages, further promoting atherosclerosis. CD40L also contributes to thrombosis and restenosis. While CD40 does not seem to affect early plaque formation, its deficiency is associated with more stable plaques at advanced stages of atherosclerosis.
Esv2n26
This document discusses the need for clinical trials targeting C-reactive protein (CRP), a marker of inflammation, in cardiovascular disease. It summarizes previous research showing that CRP levels predict future cardiovascular events and are reduced by treatments like statins and aspirin. The document calls for either a "CRP-lowering trial" to test therapies aimed at specifically reducing CRP or a "CRP-guided trial" to tailor cardiovascular treatments based on monitoring CRP levels over time. Both approaches could help develop more targeted anti-inflammatory strategies for treating heart disease.
Arterial remodeling in st vs. unst coronary synd schoenhagen1
Arterial remodeling in st vs. unst coronary synd schoenhagen1Society for Heart Attack Prevention and Eradication
This study used intravascular ultrasound to examine arterial remodeling and plaque characteristics in 131 patients with either stable angina or recent unstable symptoms. Patients with unstable presentations had greater plaque burden at the culprit lesion despite similar luminal narrowing, and a greater extent of positive arterial remodeling compared to those with stable angina. The culprit lesions in unstable patients also showed a higher rate of echolucent plaque morphology. These findings suggest that larger plaque burdens with positive remodeling may render lesions more prone to rupture and acute coronary syndromes in unstable patients.Kwong
MRI can effectively evaluate patients presenting to the emergency department with possible acute coronary syndrome. In a study of 161 such patients, MRI had higher sensitivity and specificity than electrocardiography, troponin levels, or clinical risk scores for detecting acute coronary syndrome, non-ST elevation myocardial infarction, and ischemic heart disease. Regional wall motion abnormalities detected by MRI had 89% sensitivity and 99% specificity for detecting ischemic heart disease compared to 67% sensitivity and 99% specificity for detecting ischemic heart disease using delayed hyperenhancement. MRI provides accurate information to guide patient management in the emergency department.
Esv3n11
- Nanotechnology shows promise for combining molecular imaging and targeted drug delivery for vulnerable plaques. Molecular imaging aims to enhance detection of pathologies by targeting disease biomarkers. MRI and CT are imaging modalities that could track molecular phenomena using nanoparticle contrast agents. ICAM-1 is proposed as an attractive target for delivering anti-thrombotic and anti-inflammatory drugs to vascular beds due to its expression on endothelial lumens. Future in vivo studies are needed to evaluate this new therapeutic approach of targeting ICAM-1.
Esv2n36
This document summarizes a study examining the effect of statin therapy on the progression of coronary artery calcification. The study found that patients treated with cerivastatin had a significantly lower median increase (8.8%) in coronary calcium scores compared to untreated patients (25% increase). Patients whose LDL cholesterol was reduced to under 100 mg/dl by treatment had an average decrease in calcium scores (-3.4%). The results suggest that statin therapy can slow the progression of calcification and underlying atherosclerosis. However, limitations include the open-label and prematurely ended nature of the study.
168 catheter based detection of vulnerable plaque
168 catheter based detection of vulnerable plaqueSociety for Heart Attack Prevention and Eradication
This document discusses various methods for detecting vulnerable plaque, including thermography, intravascular MRI, optical coherence tomography, angioscopy, near IR, catheter-based detection, and IVUS. It also lists types of studies that can be used for validating diagnoses and treatments of vulnerable plaque, including autopsy specimens, animal models, and human studies. Finally, it proposes a trial to detect and treat vulnerable plaque using a vulnerability detector to identify patients with vulnerable plaque and randomly assign treatment versus no treatment to measure outcomes like heart attack and sudden cardiac death.Acc 2002 mehran for print
This document discusses the use of DNA microarrays in researching vulnerable plaque. DNA microarrays allow high-throughput analysis of gene expression and have opened doors to exploring unknown molecular mechanisms. The author's research group is conducting genomic and proteomic experiments on human atherosclerotic plaques to shed light on the molecular mechanisms involved in atherosclerosis development and vulnerability. Proteomic analysis provides insights not available through genomics alone. Understanding these molecular processes could lead to better understanding of vulnerable plaque development and complications.
Es v2n19
PTX3 is a newly discovered marker of the acute phase response that is distinct from C-reactive protein (CRP) in several key ways. Unlike CRP, which is produced mainly in the liver, PTX3 is produced extrahepatically by cells involved in inflammation. Studies have found PTX3 is expressed in atherosclerotic plaques, cardiovascular tissue during heart attacks, and joints of rheumatoid arthritis patients. PTX3 may be a more specific marker of vascular inflammation than CRP due to its extrahepatic production and presence in plaques. Research also indicates PTX3 contributes to plaque vulnerability by increasing tissue factor activity and reducing clearance of apoptotic cells.
Esv2n39
This study investigated whether statin therapy can slow or reverse coronary calcification in hyperlipidemic patients. 72 patients underwent electron beam tomography scans at years 1 and 2: the first year with no lipid treatment, the second year taking cerivastatin. Cerivastatin significantly reduced LDL cholesterol and slowed the progression of coronary calcification, with calcification increasing 25% in year 1 but only 8.8% in year 2. While reversal was not seen in the whole group, patients achieving an LDL <100 mg/dl had a slight average decrease in calcification. The study demonstrated that statins can significantly slow the plaque calcification process.
Esv3n3
The document discusses the roles of Liver X receptors (LXRs) and peroxisome proliferator-activated receptors (PPARs) in regulating matrix metalloproteinase-9 (MMP-9) expression in macrophages and their implications in atherosclerosis. It reports that LXR and PPAR activation inhibits MMP-9 expression, reducing foam cell accumulation and atherosclerosis progression in mice studies. While PPARγ ligands suppress MMP-9 even in PPARγ deficient cells, the mechanisms of this effect and whether LXR ligands similarly regulate MMP-9 in LXR deficient cells requires further investigation. The LXR agonist GW3965 may have potential for stabilizing vulnerable atherosclerotic plaques by downregulating
Final clickable pps for vp s ymposium aha 2001
This document provides an overview of vulnerable plaque and summarizes the work of pioneers in the field. It describes the different types of vulnerable plaque, such as rupture-prone plaques and eroded plaques. Emerging techniques for detecting vulnerable plaque are also discussed, including intravascular ultrasound, optical coherence tomography, thermography, and various forms of spectroscopy and imaging. The goal is to noninvasively identify high-risk plaques to prevent heart attacks.
Everybody has atherosclerosis
This document discusses the history and evolution of understanding vulnerable plaque. It describes how Muller coined the term "vulnerable plaque" in 1994 to describe plaques prone to rupture. Autopsy studies in the 1980s-1990s identified characteristics of culprit plaques that cause heart attacks. Emerging diagnostic techniques like MRI, ultrasound, and thermography aim to non-invasively identify vulnerable plaque to predict cardiac events. The document outlines ongoing research exploring new methods to detect plaque inflammation and vulnerability.
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Arterial remodeling in st vs. unst coronary synd schoenhagen1
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501 autoimmune disease
1. Autoimmune reactions against heat shock proteins (HSPs), particularly HSP60, may play an important role in the early development of atherosclerosis.
2. HSPs released from necrotic cells in advanced atherosclerotic plaques can stimulate the innate immune response and promote inflammation, attracting more inflammatory cells. This may link HSPs to complications like plaque rupture and thrombosis.
3. Both humoral and cellular immune reactions against HSP60 work together with classical cardiovascular risk factors to promote atherosclerosis and its complications.
243 b cell
I. The document summarizes several studies that investigated the role of the immune system, particularly B cells, in atherosclerosis using mouse models.
II. One study found that RAG-1 deficient mice, which lack functional B and T cells, exhibited increased neointimal formation following arterial injury compared to wild type mice. Transferring B cells from wild type mice to RAG-1 deficient mice reduced neointimal formation.
III. Overall, the studies suggest that B cells may play a protective role against atherosclerosis by reducing plaque formation and progression. The mechanism may involve antibodies that target oxidation-specific epitopes, but this requires further investigation.
Atherosclerosis: New Insights on Foamy Macrophage Induction and Persistence
It is commonly assumed high cholesterol contributes to atherosclerosis which initiates with foamy macrophages. Here it is suggested the induction of foam in human macrophages relates instead to the induction of a newly described foamy virus, human endogenous retrovirus K102 (HERV-K102) in response to high cortisol and/or viruses, other intracellular pathogens, or tumors. HERV-K102 is a newly described human host protection mechanism and the particles are replication competent in vitro and in vivo. In healthy or younger adults, the foamy macrophages lyse on day 7 and release the protective HERV-K102 particles. When immunosenescence is evident (associated with low DHEA and high cortisol) the lysis and release of the HERV-K102 particles is blocked by alpha-fetoprotein (AFP). The dysfunctional and partly activated macrophages promote immunosenescence including atherosclerosis. See Laderoute MP, Discovery Medicine article published December 2015 for more details.
J Immunol-2008-Pulecio-1135-42
1) WASp-deficient dendritic cells (DCs) show impaired activation of naive CD8+ T cells, especially at low antigen doses.
2) This is partly due to altered trafficking of antigen-bearing DCs from the periphery to lymph nodes. However, correcting DC migration does not fully rescue T cell activation.
3) In vitro and in vivo imaging revealed that cytoskeletal alterations in WASp-null DCs reduce their ability to form and maintain conjugates with naive CD8+ T cells in lymph nodes, contributing to defective T cell priming.
Rheumatic feve 2018
Rheumatic heart disease is a major health problem in developing countries caused by heart lesions following rheumatic fever episodes in 30-45% of patients with untreated strep throat infections. Rheumatic fever results from an autoimmune reaction triggered by strep throat that leads to valvular damage in genetically susceptible individuals. Molecular mimicry between proteins in the streptococcus bacteria and human heart proteins is thought to underlie the pathogenesis of rheumatic heart disease.
178 vaccination against atherosclerosis
There is promising research into developing vaccines against atherosclerosis. Studies have found that vaccination against oxidized LDL and certain ApoB-100 peptides can reduce the development of atherosclerosis in animal models by up to 60%. A recent study immunized ApoE null mice with ApoB-100 peptide sequences and found a 60% reduction in atherosclerotic plaque in the aorta. Further research is still needed but vaccination shows potential as a way to prevent atherosclerosis and vulnerable plaques in humans. International collaboration could help advance this area towards developing heart attack prevention through immune modulation.
178 vaccination against atherosclerosis
Vaccination against atherosclerosis shows promise as an exciting new therapy. Studies in animal models have found that vaccination against oxidized LDL or specific ApoB-100 peptides can significantly reduce atherosclerosis. This study investigated immunization with novel ApoB-100 peptide sequences in ApoE null mice. It found a 60% reduction in atherosclerotic plaque in the aorta of immunized mice, along with increased collagen content in plaques. While more research is still needed, these results suggest that targeted vaccination against antigens involved in atherosclerosis, such as specific oxidized LDL peptides, could potentially be developed into a novel strategy for preventing heart attacks.
Esv3n12
Vaccination against atherosclerosis shows promise as an exciting new therapy. Studies in animal models have found that vaccination against oxidized LDL or specific ApoB-100 peptides can significantly reduce atherosclerosis. This study investigated immunization with novel ApoB-100 peptide sequences in ApoE null mice. It found a 60% reduction in atherosclerotic plaque in the aorta of immunized mice, along with increased collagen content in plaques. While more research is still needed, these results suggest that targeted vaccination against antigens involved in atherosclerosis, such as specific oxidized LDL peptides, could potentially be developed into a novel strategy for preventing heart attacks and strokes.
1.6 marc lecuit
1. The document discusses studying host-pathogen interactions from a clinical perspective, focusing on Listeria monocytogenes, Group B Streptococcus, and Chikungunya virus.
2. It addresses microbial species specificity, with L. monocytogenes as an example, and the importance of rational design of relevant animal models.
3. Key topics covered include microbial crossing of host barriers, microbial and host biodiversity, and the need for a holistic view of the infectious process that considers the microbial, host, and environmental factors.
ANA498Y_Final
This study aimed to differentiate between invasive squamous cell carcinoma (SCC) and carcinoma-in-situ (CIS) of the uterine cervix using immunohistochemical markers. Tissue samples from 37 patients were stained for CD3, CD4, CD8, CD20, and CD138. Scoring showed decreased expression of CD8, CD20, and CD138 in invasive SCC compared to CIS, indicating differences in immune cell infiltration between invasive and non-invasive lesions. The results provide potential markers for differentiating invasive SCC from CIS of the cervix.
USP CHOP Annie De Groot Presentation June 2013
This document discusses residual host cell proteins (HCPs) in therapeutic protein formulations and their potential impact on immunogenicity. It provides several examples showing how minor mismatches between species sequences can lead to an immune response. The key points are that T cell epitopes drive immunogenicity, and proteins that are normally self-tolerated can become immunogenic if they contain T cell epitopes foreign to the patient. HCPs from CHO cell lines used in production may contain such non-self epitopes and have canceled clinical trials due to unexpected immune responses against CHO components. A thorough immunoinformatics analysis of contaminating proteins is important to understand and mitigate immunogenicity risks.
075 immune modulation
This document discusses potential immune-based therapies for modulating atherosclerosis and vulnerable plaque. It suggests that targeting specific antigens, co-stimulatory molecules, cytokines, vaccines, recombinant proteins, antibodies, cells, or small molecule drugs could help shift the immune response away from pathogenic Th1 immunity toward protective Th2 immunity. Several approaches show promise in animal models, including immunization with oxidized LDL to induce protective antibodies, administration of the heat shock protein HSP65 to reduce lesions, and use of pentoxifyllin or statins which can inhibit Th1 responses and atherosclerosis. However, challenges remain in translating these strategies to chronic human disease given general immunosuppression carries side effects from increased infection risk.
Rheumatic feve 2018
Rheumatic heart disease is a major health problem in many developing countries. It results from autoimmune reactions triggered by untreated streptococcal throat infections, leading to valvular damage. Genetics play a role in susceptibility. The pathogenesis involves molecular mimicry between antigens in group A streptococcus bacteria and human proteins, which can induce cross-reactive antibody responses and result in autoimmune-mediated damage to heart valves and other tissues. Cytokines and specific immune responses are also involved in the progression of rheumatic heart disease.
Guillain Barre Syndrome
Guillain Barre Syndrome (GBS) is an acute immune-mediated inflammatory neuropathy. It is the most common cause of acute flaccid paralysis worldwide. Recent decades have seen progress in understanding the epidemiology, pathogenesis, and prognosis of GBS. The pathogenesis involves molecular mimicry between gangliosides and antigens from preceding infections like Campylobacter jejuni, leading to anti-ganglioside antibody production and complement-mediated nerve damage. Different GBS subtypes are associated with different antiganglioside antibodies and clinical courses.
1017.full
High-affinity interactions between antigenic peptides and heat shock protein 70 (HSP70) can enhance CD8+ T cell immune responses. A novel higher-affinity HSP70-binding sequence called J1 was introduced, which significantly improved binding of peptides to HSP70. The OVA peptide SIINFEKL modified with J1 showed a 15-fold higher affinity for HSP70 compared to the original J0 sequence. Additionally, changing the orientation and adding a cleavable linker between the binding sequence and epitope further increased immunogenicity, demonstrating enhanced immune responses with multiple mouse and human epitopes. These modified epitopes complexed with HSP70 have potential for creating successful multivalent vaccines against infectious diseases and
Baker ectrims teaching slides
This document summarizes a presentation given by Professor David Baker on B cell therapy for multiple sclerosis. It discusses B cell subsets, the role of B cells in the pathogenesis of MS, response to different therapies as a key experiment to understand biology, and repopulation characteristics of immune cells after treatment. It also provides diagrams on immune cell differentiation and repopulation, the two compartment model of treating inflammatory lesions in MS, phenotypes seen in active MS lesions, and types of monoclonal antibodies used as treatments.
J Immunol-2008-Tagliani-3201-9
This document summarizes a study that screened an antibody library to identify antibodies that could induce protective immune responses by targeting dendritic cells. The screening identified an antibody against CD36, a receptor expressed on CD8α+ dendritic cells. The antibody was linked to the model antigen OVA and shown to deliver the antigen for both MHC class I and II processing in vitro and in vivo. Immunization with the anti-CD36-OVA antibody induced robust activation of naive CD4+ and CD8+ T cells and differentiation of primed CD8+ T cells into long-term effector cytotoxic T lymphocytes. Vaccination protected against tumor growth in a tumor-specific antigen model. Targeting CD36 was qualitatively different than targeting DEC
Reactive arthritis
This document discusses reactive arthritis, beginning with the case of a 36-year-old man who was admitted to the hospital with acute arthritis in both knees after experiencing diarrhea. Reactive arthritis is defined as an infectious-induced systemic illness characterized by aseptic joint inflammation in a genetically predisposed individual following a distant bacterial infection. It commonly follows infections from bacteria like Salmonella, Shigella, Campylobacter, Yersinia, and Chlamydia. The presentation, epidemiology, pathogenesis, clinical manifestations, diagnostic criteria, treatment, and prognosis of reactive arthritis are described in detail.
Coronary Artery Disease in HIV
This document discusses coronary artery disease in HIV patients. It covers the relative magnitude of cardiovascular disease among HIV patients, current data on the association between HIV and coronary artery disease, known risk factors and how they may be modulated by HIV diagnosis, screening and prevention recommendations, and areas for future research. Key points include increased rates of myocardial infarction and atherosclerosis in HIV patients, traditional and HIV-specific risk factors, screening tools and their limitations, effects of antiretroviral therapy on risk, and lifestyle and medical interventions for prevention.
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Galinpepimut-S (WT1-targeting peptide vaccine) in high-risk multiple myeloma. Final results from a Phase 2 clinical study. Koehne G, et al. EBMT 2018 slide presentation.
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More from Society for Heart Attack Prevention and Eradication
AHA SHAPE Symposium 2017 Dr. Naghavi Presentation
AHA SHAPE Symposium 2017 Dr. Naghavi PresentationSociety for Heart Attack Prevention and Eradication
This document discusses developing an artificial intelligence system to predict short-term cardiovascular disease (CVD) events. The goal is to eradicate unexpected heart attacks by predicting risk similar to hurricane forecasts. Existing studies are cited that show over 50% of heart attacks are first symptoms of underlying disease. The document outlines previous work by SHAPE to define vulnerable patients and release guidelines. It proposes using machine learning on existing cohort data to develop algorithms predicting heart attacks within 12 months, and validate the system. The hope is this can trigger preventative actions and add over 10 years to life expectancy. Funding is needed to implement the proposed "Machine Learning Vulnerable Patient Project".AHA SHAPE Symposium 2017 Dr. Kloner Presentation
Triggers of cardiovascular events can include physical and emotional stress. Stress from events like earthquakes, blizzards, intense sporting games, and overexertion from activities like snow shoveling have been shown to increase the risk of acute cardiovascular outcomes like myocardial infarction. While modern therapies have improved cardiovascular health, research continues to show temporary increases in cardiovascular mortality associated with highly emotional sporting events even in recent years. Managing risk factors, reducing stress, and utilizing preventative therapies may help reduce the impact of triggers on cardiovascular health.
AHA SHAPE Symposium 2017 Dr. Greenland Presentation
AHA SHAPE Symposium 2017 Dr. Greenland PresentationSociety for Heart Attack Prevention and Eradication
The document introduces the All of Us Research Program, which aims to collect health data from one million Americans to advance precision medicine research. It was announced by President Obama in 2015. The program receives funding from the federal government and private partners. It collects various types of health data from participants through surveys, health records, samples, and devices. The data is stored and shared securely while protecting privacy. The goal is to generate new medical discoveries and more personalized healthcare through collaboration between researchers and participants.AHA SHAPE Symposium 2017 Dr. Yen Presentation
A machine learning model outperformed the ACC/AHA Pooled Cohort Equations Risk Calculator in detecting high-risk asymptomatic individuals and recommending statin treatment for cardiovascular disease prevention in the Multi-Ethnic Study of Atherosclerosis. The machine learning model used support vector machines and data augmentation to derive a CVD risk predictor from nine variables in the MESA study population. It demonstrated higher sensitivity, specificity, and AUC compared to the ACC/AHA risk calculator, recommending statin treatment for fewer individuals while missing fewer cardiovascular events.
AHA SHAPE Symposium 2017 Dr. Slomka Presentation
This document discusses machine learning applications in cardiac imaging presented by Piotr Slomka. It describes how machine learning can improve image analysis, diagnosis, and risk prediction. Machine learning combines multiple data points like imaging and clinical data to predict outcomes. Deep learning can perform tasks like image segmentation. Machine learning provides quantitative scores that predict disease, need for intervention, or patient outcomes to help clinicians. The goal is to integrate machine learning into clinical decision making.
Vu lplaque1 pasterkamp
This document summarizes a post-mortem study examining the prevalence of inflammatory cells in non-ruptured atherosclerotic plaques. The study found that moderate or heavy staining for macrophages was present in 45% of femoral artery cross-sections and 84% of femoral arteries had at least one cross-section with moderate/heavy inflammation. There was no observed relationship between the degree of inflammation in the left and right coronary arteries within individuals, indicating the level of local inflammation is locally determined with little predictive value for other arteries.
Vulnerable plaque vulnerable patient
The document provides guidelines for defining vulnerable plaque and vulnerable patients from the Association for Eradication of Heart Attack. It outlines major and minor histopathological and clinical criteria for vulnerable plaque including active inflammation, thin fibrous cap with large lipid core, endothelial denudation, and stenosis. Potential screening and diagnostic methods are discussed at the plaque, systemic, and blood levels ranging from non-invasive imaging to intravascular techniques. Different types of vulnerable plaque that can cause acute coronary events are also categorized.
Vulnerable plaque overview
Vulnerable plaque refers to dangerous forms of atherosclerotic plaques that can rupture or induce thrombosis, disrupting blood flow. The document discusses the history and research around vulnerable plaque, including pioneers in the field and emerging techniques to detect vulnerable plaque such as intravascular ultrasound, optical coherence tomography, and magnetic resonance imaging. It summarizes that vulnerable plaques are typically characterized by a thin fibrous cap, large lipid core, and presence of macrophages.
Vulnerable patient talk in poland
The document summarizes research on vulnerable plaques and markers of vulnerability. It finds that ruptured plaques are the most common type of culprit lesion, accounting for around 70% of cases. Major criteria for defining vulnerable plaque include outward remodeling, endothelial dysfunction, and a thin fibrous cap with a large lipid core. Both plaque morphology and activity need to be assessed to identify vulnerability.
Vulnerable patient slides without movies
This document contains a summary of a presentation on vulnerable patient syndrome. It includes PowerPoint slides and videos on defining and identifying vulnerable plaques and patients. It thanks sponsors for their support of the educational event. The slides define vulnerable plaques as those likely to rupture in the future, causing heart attacks, and provide criteria for identifying them based on morphology and activity. Biomarkers and conditions that increase plaque and myocardial vulnerability are also summarized. The presentation outlines a pyramid approach for screening, diagnosing, and treating vulnerable patients annually to help reduce heart attacks and their high costs.
Vulnerable patient mar 04
This document discusses triggers for sudden cardiac arrest (SCA) and death (SCD). It notes that over 2/3 of SCD cases are unable to be predicted due to a lack of well-established risk factors. While population risk factors can identify at-risk groups, they cannot predict risk for individuals. The document explores various biological, anatomical, and environmental factors that can precipitate fatal arrhythmias and discusses how the timing of transient initiating events is critical for the development of ventricular tachyarrhythmias. It emphasizes that myocardial electrophysiological processes likely determine the onset or lack of VT/VF/SCD and that immediate access to automated external defibrillators is needed to save lives.
Vulnerable (thrombogenic blood
This document summarizes presentations from symposia on vulnerable plaque and discusses the relationship between plaque, blood, and patients in atherothrombosis. It notes that multiple factors like diabetes, smoking, and hyperlipidemia can make blood more thrombogenic and moderate the severity of acute events after plaque rupture. Statins, aspirin, and other drugs that target tissue factor or thrombin pathways may be promising antithrombotic agents by inhibiting thrombosis initiation and propagation.
Vuln shape aha 2005
The document discusses vulnerable plaque and challenges in detecting and treating it. It describes various imaging techniques for detecting vulnerable plaque such as thermography, MRI, CT angiography, and optical coherence tomography. However, it notes that while these can identify high-risk features, it remains unclear what exactly defines vulnerable plaque and whether imaging findings truly correlate with risk. The document also notes that while statins reduce events, the relationship between plaque burden and events is unclear, and better defining and detecting the disease is still needed before new therapies can be developed.
Vuln plaque poster burke
1) The study examined 92 hearts from patients with severe coronary artery disease who died suddenly. The hearts were sectioned and plaque types were classified.
2) The number of "vulnerable" plaques, particularly thin cap atheromas, was highest in hearts of patients who died from acute plaque rupture and lowest in those with incidental disease.
3) Thin cap atheromas and other unstable plaque types were concentrated in the proximal coronary segments, similar to the distribution of plaque ruptures. The study suggests vulnerable plaques contribute to acute coronary syndromes and are non-uniformly distributed within the coronary arteries.
Vp watch editorial_slide 25short-
1) Drug-coated stents, particularly those coated with sirolimus, have shown promise in reducing restenosis compared to bare metal stents. Sirolimus inhibits cell proliferation and has been shown in studies to reduce intimal hyperplasia and restenosis in animal models by 50% or more.
2) A study by Suzuki et al. found that a sirolimus-coated stent reduced restenosis by 50% through inhibiting cellular proliferation in a dose-dependent manner compared to a bare metal stent. Adding dexamethasone to the coating did not provide additional benefit.
3) If results of the RAVEL clinical trial showing "zero" restenosis out to 5 years
Vp watch editorial_slide25
This document discusses drug-coated stents for preventing restenosis. It summarizes a study showing that stents coated with sirolimus via a polymer matrix reduced restenosis by 50% by inhibiting cell proliferation. Adding dexamethasone provided no additional benefit. Other studies also showed sirolimus inhibits smooth muscle cell proliferation. If results of the RAVEL trial showing "zero" restenosis at 210 days hold true long-term, sirolimus-coated stents may become the standard therapy for coronary revascularization. Questions are raised about whether coating vulnerable plaques could be a primary treatment and if multiple vulnerable plaques would all be stented.
Vp watch editorial_slide25short-
1) Drug-coated stents, particularly those coated with sirolimus, have shown promise in reducing restenosis compared to bare metal stents. Sirolimus inhibits cell proliferation and has been shown in studies to reduce intimal hyperplasia and restenosis in animal models by 50% or more.
2) A study by Suzuki et al. found that a sirolimus-coated stent reduced restenosis by 50% through inhibiting cellular proliferation in a dose-dependent manner compared to a bare metal stent. Adding dexamethasone to the coating did not provide additional benefit.
3) If results of the RAVEL clinical trial showing "zero" restenosis out to 5 years
Vp watch2002
I. This document discusses various animal models that have been used to study atherosclerosis and plaque rupture, including quail, pigeons, chickens, dogs, monkeys, pigs, rats, rabbits, and mice. It provides details on the types of lesions developed and similarities to human disease for each model.
II. The double knockout LDL/apoE mice are highlighted as offering improvements in studying clinical complications of atherosclerosis like human heart disease. However, it is unclear how closely they model vulnerable plaques.
III. Questions are raised about how closely the coagulation systems of these animal models resemble humans and whether any model fully captures repeated plaque ruptures and the role of aging in natural history as seen in humans.
Vp symposium31602
Trans-Blood Vision is a patented infrared technique that uses short-wave infrared wavelengths to see directly through blood. It has the potential to find vulnerable plaque lesions without first entering them, determine their size and surface characteristics in high resolution, and look at their material constituents both on and below the surface. While it cannot provide direct visual guidance for therapy or penetrate as deeply as ultrasound, combining it with augmentative technologies could allow for real-time multi-mode detection, analysis, and therapy guidance of vulnerable plaque lesions. The document concludes that Trans-Blood Vision warrants significant investigation, possibly in combination with other emerging technologies.
Vpschoenhagen
This study used intravascular ultrasound to examine arterial remodeling and plaque characteristics in 131 patients with either stable angina or recent unstable symptoms. Patients with unstable presentations had greater plaque burden at the culprit lesion despite similar luminal narrowing, and a greater extent of positive arterial remodeling compared to those with stable angina. The culprit lesions in unstable patients also showed a higher rate of echolucent plaque morphology. This suggests that bulky, remodeled plaques may be more vulnerable to rupture, leading to acute coronary syndromes. Further prospective study is needed to better understand the relationship between clinical presentation and plaque features.
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Esv2n49
- 1. HSP-65, An Autoantigen for Plaque Development or Plaque Vulnerability? Editorial Slides VP Watch – December 11, 2002 - Volume 2, Issue 49 Yehuda Shoenfeld, MD Sheba Medical Center, Tel Hashomer,Israel
- 2. A large number of studies have been reported on associations of coronary artery disease (CAD) in human and certain persistent bacterial and viral infections. 1
- 3. In 1978, Fabricant et al showed that experimental infection of germ-free chickens with an avian herpes virus induces arterial disease that resembles human atherosclerosis. 2
- 4. Atherosclerosis as an Autoimmune Disease Autoantigens: - Oxidized LDL - Heat Shock Protein 65 - β2 Glycoprotein I - ???
- 5. Traditional Framingham risk factors fail to fully account for accelerated atherosclerosis in systemic lupus erythematosus. 3
- 6. Criteria Needed to Establish An Autoimmune Etiology. Witebsky-Rose criteria 4 It should be possible to: 1. Demonstrate immunological reactivity to a self-antigen. Characterize or isolate the inciting autoantigen. 2. Induce immunological reactivity against that same antigen by immunization of experimental animals. 3. Show pathological changes (similar or identical to those found in human disease) in the appropriate organs/tissues of an actively-sensitized animal. 4. As in 4 but following passive transfer of auto-Abs or auto- reactive T cells.
- 7. Human heat shock proteins (HSPs) are expressed on endothelial cells in response to stressors such as hypertension, smoking, lipoproteins - etc. 5 HSPs offer a target for autoimmunity under such circumstances. 5
- 8. Anti-HSP-65 and Atherosclerosis Carotid atherosclerosis Coronary heart disease Myocardial infarction Arteriosclerosis Coronary angioplasty Myocardial infarction
- 9. Expression Of Heat Shock Protein- 70 By Dendritic Cells In early intimal lesions, HSP70 is over-expressed exclusively by dendritic cells, which suggests that dendritic cells might be involved in the early phases of atherogenesis. 6
- 10. T Lymphocytes in atheroma 20% of the infiltrating inflammatory cells are T-lymphocytes. 6, 7 T- lymphocytes are in an activated state; memory cells, CD4+ TCRab +. 6, 7
- 11. Enhanced fatty formation in C57BL/6J mice by immunization with heat shock protein-65 Jacob George, Yehuda Shoenfeld, Arnon Afek, Boris Gilbourd, Pnina Keren, Aviv Shaish, Juri Kopolovic, George Wick, Dror Harats Arterioscler Thromb Vasc Biol,19:505- 510,1999
- 14. Cellular and Humoral Immune Responses to Heat- Shock Protein 65 Are Both Involved In Promoting Fatty-Streak Formation In LDL- Receptor Deficient Mice Jacob George, Aron Afek, Boris Gilburd, Yehuda Shoenfeld, Dror Harats. J Am Coll Cardiol 2001; 38: 900-905. Antibodies and lymphocytes reactive to HSP65 promote fatty-streak formation in mice, providing direct evidence for the proatherogenic properties of cellular and humoral immunity to HSP65.
- 15. Adoptive transfer of β2 glycoprotein I (β2GPI) reactive lymphocytes enhances early atherosclerosis in LDL-receptor deficient mice * Lymphocytes obtained from draining LN (mostly T cells) and splenocytes increased atherogenesis. * Deletion of T cells prevented atherogenesis. * Ultimate evidence for autoimmunity and immune system in atherosclerosis. * Importance of T cells in the process. Jacob George, Dror Harats, Boris Gilburd, Arnon Afek, Aviv Shaish, Juri Kopolovic, Yehuda Shoenfeld. Circulation 102: 1822 - 1827, 2000.
- 16. Atherogenesis Plaque Rupture Thrombosis Infection of arterial wall - SMC proliferation associated with p53 inactivation - Local inflammation Systemic Infection – Endothelial dysfunction due to circulating endotoxin Classic risk factors ↓ HDL Fibrinogen Triglycerides Autoimmunity - HSP60 cross-reactivity with bacterial antigens Systemic inflammation CRP Leukocyte count Cytokines Adapted from: J. Danesh et al. Chronic infection and coronary heart disease: is there a link?. Lancet 350 (1997), pp. 430–436. Postulated Mechanisms to Link Infections And Vascular Disease
- 17. As reported in VP Watch this week, Lamb et al used a BCG immunization model to assess the role of HSP in the association between infection and CAD. 7
- 18. They immunized rabbits with BCG vaccine (n=10) or saline (n=10) and subsequently fed a cholesterol diet for 10 weeks. 7 Plasma IgG specific for mycobacterial antigen A60 and human HSP-60, but not for human HSP-70, rose following BCG immunization, reaching a peak after 8 weeks. 7
- 19. 0 10 20 30 40 BCG Control BCG Control %aorticareacovered P<0.05 The percentage aortic area staining positively for oil red O was calculated. Each point is the mean±SE for seven rabbits. Statistical analysis was performed using unpaired t-tests. *P<0.05. * Effect of BCG immunization on atherosclerosis in thoracic aorta of cholesterol-fed rabbits Lamb DJ, Ferns GA. The magnitude of the immune response to heat shock protein-65 following BCG immunization is associated with the extent of experimental atherosclerosis. Atherosclerosis. 2002 Dec;165(2):231-40.
- 20. The percentage aortic area covered by atherosclerotic plaque was greater in animals immunized with BCG compared to controls.7 The authors did not find any correlation between anti-A60 antibody titers and plaque area. 7
- 21. Conclusion: Immunization with an HSP-containing BCG vaccine, using doses equivalent to those used for tuberculosis prophylaxis, has pro-atherogenic consequences in the cholesterol-fed rabbits. This effect may be mediated in part by immune response directed against BCG-associated HSP.
- 22. Questions: - Is heat shock protein 65 the main culprit autoantigen for atherosclerosis? - Knowing the role of HSP-65 in other autoimmune diseases such as rheumatoid arthritis, how specific can HSP-65 be for atherosclerosis?
- 23. Questions: Should we look for a single specific antigen for atherosclerosis in all patients? Or do different antigens exist in different patients or even within the same patient?
- 24. Questions: Do you think that the role of these autoantigens may vary at different stages of the disease? Do you think that some may contribute to plaque development and others may induce plaque complication? Knowing that high LDL is necessary for atherosclerosis and HSP only enhances atherosclerosis, is it appropriate to say that HSP-65 may be more important in plaque complication (vulnerability) than plaque generation?
- 25. 1) J. Danesh, R. Collins and R. Peto , Chronic infection and coronary heart disease: is there a link?. Lancet 350 (1997), pp. 430–436. 2) CG Fabricant, J Fabricant, MM Litrenta and CR Minick, Virus-induced atherosclerosis. J Exp Med 148 (1978), pp. 335– 340. 3) Esdaile JM, et al Arthritis Rheum 2001, 44: 2311-7 4) Krenn V, Souto-Carneiro MM, Kim HJ, Berek C, Starostik P, Konig A, Harms H, Muller-Hermelink HK Histopathology and molecular pathology of synovial B-lymphocytes in rheumatoid arthritis. Histol Histopathol. 2000 Jul;15(3):791-8. Review. 5) George J, Harats D, Shoenfeld Y.Clin Rev Allergy & Immunol. 18: 73-86, 2000. 6) Bobryshev YV, Lord RS. J Vascular Surgery 35: 368-75, 2002 7) A. Kinnunen et al. Scand J Immunol 2001; 54: 76-81. 8) Lamb DJ, Ferns GA.The magnitude of the immune response to heat shock protein-65 following BCG immunisation is associated with the extent of experimental atherosclerosis. Atherosclerosis. 2002 Dec;165(2):231-40. References