189 hsp 65
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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 immunization with HSP-65 can enhance atherosclerosis in cholesterol-fed rabbits. 3. While HSP-65 may contribute to plaque development and vulnerability, the role of autoantigens in atherosclerosis is complex. Different antigens could be involved
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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.
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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.
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.
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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.
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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.
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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.
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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
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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.
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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.
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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 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.
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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.
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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.
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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
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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.
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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.
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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.
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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.
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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.
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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.
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1. Autoimmune reactions against heat shock proteins (HSPs), particularly HSP60, may play an important role in the early development of atherosclerosis.
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3. Both humoral and cellular immune reactions against HSP60 work together with classical cardiovascular risk factors to promote atherosclerosis and its complications.
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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.
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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
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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.
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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.
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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.
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This document summarizes research on using optical coherence tomography (OCT) to characterize coronary plaques. OCT uses near-infrared light to generate high-resolution cross-sectional images of tissue microstructure. Researchers studied 357 arterial segments ex vivo using OCT and validated plaque types (fibrous, calcific, lipid-rich) against histology with high accuracy. A pilot clinical study of 10 patients found OCT feasible and safe for in vivo coronary imaging before and after percutaneous coronary intervention, identifying a variety of plaque types and stent appositions. While blood obstruction and motion artifacts posed challenges, the results support further evaluation of OCT as a potential "optical biopsy" tool.
131 the evolution of coronary atherosclerosis
The document discusses the natural progression of coronary atherosclerosis over time from normal artery to vulnerable plaque. It describes how snapshots can identify plaque vulnerability or likelihood to progress. Physiologic shear stress is protective for endothelium while low shear stress promotes atherosclerosis. 3D reconstruction of arterial segments can analyze plaque and shear stress. Regions of baseline low shear stress saw increased plaque and arterial enlargement over 6 months. Identification of minor obstructions likely to progress could allow preventive interventions to avert adverse events like heart attack.
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.
147 vulnerable thrombogenic blood
This editorial discusses factors that influence whether a ruptured atherosclerotic plaque leads to a coronary thrombosis. It reports on a study that found increased levels of circulating tissue factor activity in poorly-controlled type 2 diabetics, smokers, and hyperlipidemic patients. This tissue factor increases blood thrombogenicity and correlates with an increased risk of atherothrombotic complications in these populations. The authors conclude that improved glycemic control in diabetics reduces tissue factor levels and thrombogenicity. Risk factors such as smoking and hyperlipidemia increase tissue factor and thrombogenicity levels.
159 spio uptake by macrophages
This document describes a study comparing four types of superparamagnetic iron oxide (SPIO) nanoparticles and their ability to be taken up by macrophages and detect plaque inflammation via MRI. The study finds that lipid-coated SPIO-2 is taken up strongly by macrophages, induces less oxidative stress than dextran-coated SPIO, and is not inhibited by a mannose receptor inhibitor. SPIO-2 therefore shows potential as a contrast agent for noninvasive MR imaging of vulnerable atherosclerotic plaques containing macrophage inflammation. Such detection could help identify high-risk patients and reduce deaths from heart attacks and strokes.
Coronary artery disease among asymptomatic diabetic and non-diabetic patients...
This study aimed to determine the prevalence and severity of coronary artery disease (CAD) in asymptomatic diabetic and nondiabetic patients using coronary CT angiography (CCTA). The study found CAD was present in 93% of asymptomatic diabetics compared to 73% of nondiabetics. Obstructive CAD was more common in diabetics at 29% versus 6.6% in nondiabetics. Diabetics also had higher total Agatston scores and more coronary segments with atherosclerosis. The results indicate asymptomatic diabetics have a high prevalence of CAD, suggesting CCTA may be useful for evaluating subclinical disease in this high risk group.
191 spio and t2 effect
The study aimed to show the effect of macrophage uptake of superparamagnetic iron oxide (SPIO) nanoparticles on T2 relaxation time in vitro. Macrophages were incubated with different concentrations of Feridex, an SPIO contrast agent, for varying time periods. T2 relaxation times were measured after 20 minutes, 1 hour, 6 hours, and 24 hours. T2 values decreased with both increasing SPIO concentration and longer incubation time, demonstrating concentration- and time-dependent SPIO uptake by macrophages and corresponding reduction in T2 signal.
199 plaque severity and coronary occlusion
The document discusses that less obstructive plaques pose a greater risk of coronary occlusion than severely obstructed plaques due to their greater numbers. It also states that the aggregate risk of rupture from many non-significant lesions exceeds that of fewer significant lesions, so a myocardial infarction is more likely to originate from a non-significant lesion. Additionally, while electron beam tomography (EBT) cannot identify vulnerable plaques directly, it can identify vulnerable patients based on their coronary artery calcium (CAC) scores and percentiles, as risk increases with higher scores. EBT is also useful for estimating prognosis and tracking changes in plaque burden in response to treatment over time.
124 nitrate tolerance
Nitrate tolerance occurs due to decreased nitric oxide activity in the body and activation of counterregulatory mechanisms like neurohormonal activation and plasma volume expansion. Glyceryl trinitrate increases matrix metalloproteinase activity. Studies show the worst survival rates after myocardial infarction in patients treated with nitrates.
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Similar to 189 hsp 65
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: 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.
Ebmt 2018 gps in mm koehne et al_with suppl slides_final_final_1.1.12_mar2018...
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.
Es v2n45
Virus-infected monocytes can initiate coagulation and promote inflammation. An in vitro study found that monocytes infected with cytomegalovirus, influenza A virus, or Chlamydia pneumoniae expressed tissue factor and reduced clotting time, indicating initiation of coagulation. The viruses also stimulated monocytes to produce inflammatory cytokines like IL-6 and IL-8. While all three viruses infected monocytes, influenza A most strongly induced cytokine production. This suggests virus-infected monocytes may contribute to both acute coronary events by promoting plaque instability and the chronic atherosclerosis process through sustained inflammation and coagulation.
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Atherosclerosis: New Insights on Foamy Macrophage Induction and Persistence
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This document provides background on Jacques Barth, an expert in cardiovascular imaging and risk assessment. It discusses the evolution of ultrasound technology for measuring intima-media thickness (IMT) from 1986 to 2005. IMT is an early marker of atherosclerosis and cardiovascular risk. The document also addresses issues around vulnerable plaques, reporting IMT measurements, and assessing cardiovascular risk in children and adolescents.
Braunwald
This document outlines an approach to identifying and managing coronary risk. It recommends that prevention must be the primary goal through intensive global risk factor reduction for all patients with clinically apparent heart disease. It also recommends identifying asymptomatic high-risk individuals through testing like the Framingham Risk Score so they can receive prevention. It proposes a risk stratification approach from low to very high risk based on annual risk levels and corresponding testing and treatments, with very high risk patients receiving the most intensive treatments like invasive detection of unstable plaques and procedures like CABG or multiple drug-eluting stents.
Acc vp-org 3-02 stone
This document describes a study that uses intravascular ultrasound (IVUS), biplane coronary angiography, and blood flow measurements to characterize endothelial shear stress (ESS) in coronary arteries. It found that over 6 months, areas of low ESS demonstrated plaque progression, areas of normal ESS remained stable, and areas of high ESS developed outward remodeling. The technology allows in vivo determination of intracoronary flow velocity and ESS, which has not previously been possible. This provides a method to predict progression of atherosclerosis and vascular remodeling. A pilot study applied this technique in 8 patients at baseline and 6 months to analyze changes in native coronary artery disease and in-stent restenosis while taking candesartan vs fel
101205 shape aha 2005 f
Zahi A. Fayad is an Associate Professor who studies molecular imaging of atherosclerosis using MRI. His research focuses on developing targeted contrast agents to noninvasively detect unstable plaque. Some agents under investigation include annexin A5 labeled with a radioisotope to detect apoptosis, FDG-PET to assess plaque activity, and fibrin-targeted and MMP-targeting Gd-based contrasts. Additional work involves lipid-based particulate agents using reconstituted HDL or iron oxide nanoparticles. The goal is to improve MRI detection sensitivity and specificity for high-risk plaque characterization.
Acc v porg becker
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Acc 2005-1, v pl-vp
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Acc presentation macrophage (1)
This document proposes a non-invasive method using SPIO (super paramagnetic iron oxide) nanoparticles to image macrophage infiltration and inflammation in vulnerable atherosclerotic plaques. Rabbits and mice were injected with SPIO, which accumulated in inflamed plaque areas correlated with macrophage density. SPIO-enhanced MRI then successfully identified these inflamed plaques non-invasively in vivo. This technique could provide a way to detect rupture-prone plaques and better understand plaque vulnerability.
Acc v porg
This document discusses the use of coronary CT angiography (CTA) to detect and characterize coronary atherosclerosis beyond just detecting coronary stenoses. CTA can identify calcified plaques, non-calcified plaques, and mixed plaques. It can detect atheromas and characterize plaque density. CTA can also identify intracoronary thrombi and myocardial infarction scars. The document outlines the CTA scanning parameters and techniques used to minimize motion artifacts and optimize image quality for plaque detection and characterization.
Acc presentation (1)
This document describes a study that introduces a non-invasive method for imaging macrophage infiltration in inflamed atherosclerotic plaques using superparamagnetic iron oxide (SPIO) nanoparticles and MRI. The researchers injected SPIO into hypercholesterolemic and normal rabbits and found that SPIO profoundly accumulated in areas of macrophage infiltration in the atherosclerotic plaques, as confirmed by histology. SPIO-enhanced MRI was able to identify these inflamed plaques non-invasively. The results suggest SPIO-enhanced MRI can be a novel method for detecting rupture-prone inflamed plaques associated with heart attacks and strokes.
Ac cculprit
The document discusses several factors that are considered predictors of plaque vulnerability, including luminal narrowing, plaque volume and composition, fibrous cap thickness, and plaque inflammation. It reviews studies that show myocardial infarction can develop from previously non-severe lesions and that lipid content, cap thickness, inflammation, and stress factors like circumferential stress are correlated with plaque stability and vulnerability. In conclusion, the size and composition of the lipid core, thickness and composition of the fibrous cap, and inflammation are well-established predictors of plaque rupture.
Acc presentation lipid coated(2)
This document discusses a novel tracer for MRI imaging of macrophage infiltration in atherosclerotic plaque. It summarizes research into lipid-coated superparamagnetic iron oxide nanoparticles (SPIOs) that are phagocytosed by macrophages. The researchers tested various SPIO coatings and sizes to maximize macrophage uptake while minimizing oxidative stress. Lipid-coated SPIOs combined with certain aminoglycans showed the highest uptake and lowest induction of reactive oxygen species. The goal is to develop an MRI contrast agent that can noninvasively image vulnerable, inflamed plaques by detecting macrophage presence.
Acc 2002 microarray mehran for print
This document discusses the use of DNA microarrays in vulnerable plaque research. It provides background on atherosclerosis and identifies DNA microarrays as a tool that can be used to investigate the molecular mechanisms underlying plaque vulnerability. The document outlines the basic steps of a DNA microarray experiment and discusses considerations for experimental design, data analysis, and validation of results. It also summarizes several studies that have used DNA microarrays or related techniques to examine gene expression in atherosclerosis.
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Acc 04 vuln pt
This document discusses approaches to identifying and managing coronary risk. It states that the primary goal should be preventing acute cardiac events through intensive risk factor reduction for all patients with clinically apparent heart disease. Additionally, it notes that one third of sudden cardiac deaths and heart attacks occur in previously asymptomatic individuals with undiagnosed risk factors or pre-clinical disease. The document proposes identifying high-risk asymptomatic individuals through testing to provide prevention. It presents a risk stratification approach using testing like CRP, cholesterol, glucose and imaging to guide different levels of risk factor reduction and management.
Acc 2002 mehran for print
This document discusses the use of DNA microarrays in studying vulnerable atherosclerotic plaques. It provides background on atherosclerosis and plaque rupture. DNA microarrays allow high-throughput analysis of gene and protein expression, which can provide insights into molecular mechanisms underlying plaque vulnerability. One study used microarrays to analyze gene expression differences between ruptured and stable plaques, identifying perilipin as upregulated in ruptured plaques. However, microarray analysis of atherosclerosis is still in its early stages with many technical challenges to address.
Acc2002 thermography
Vulnerable plaques are prone to rupture and cause heart attacks. This document proposes criteria for defining vulnerable plaques based on histopathology and clinical factors. It also explores using infrared thermography to identify vulnerable plaques by detecting heat from macrophage inflammation. Studies in animal models and humans found temperature heterogeneity in atherosclerotic arteries that correlated with plaque vulnerability features. Further research aims to develop non-invasive thermography techniques to accurately detect vulnerable plaques and help predict heart attack risk.
A20 gene
The document presents findings on the A20 gene, which encodes a zinc finger protein that inhibits NF-kB activity and TNF-induced apoptosis. The study found that C57 and FVB mouse strains have a coding difference in A20 that generates a phosphorylation site in C57 mice. C57-A20 was less effective at shutting down TNF-induced NF-kB activity and C57 cells were less susceptible to TNF-induced apoptosis compared to FVB cells. This suggests less active A20 in C57 mice leads to increased inflammation and reduced apoptosis, while more active A20 in FVB mice decreases inflammation and increases apoptosis, contributing to differences in atherosclerosis susceptibility between the strains.
#1 killer of human beings in the 21st century
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.
A20 is an atherosclerosis
The document presents findings on the A20 gene, which encodes a zinc finger protein that inhibits NF-kB activity and TNF-induced apoptosis. The study found that C57 and FVB mouse strains have a coding difference in A20 that generates a putative phosphorylation site in C57 mice. Experiments showed the C57 version of A20 is less effective at shutting down NF-kB activity and C57 cells are less susceptible to TNF-induced apoptosis. This suggests the A20 variation could contribute to differences in atherosclerosis susceptibility between C57 and FVB strains by affecting inflammation and apoptosis.
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189 hsp 65
- 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