That’s important because right now, doctors have to rely on a set of 11 criteria, which can overlap with many other diseases, to try to make a diagnosis.
“It is one of the most complex clinical diagnoses,” says Pascual, who is also a practicing pediatric rheumatologist.
“It might lead to better diagnostic tests, but we don’t know that yet,” Pascual says. Other experts say the discoveries will most certainly lead to new drug targets.
Systemic lupus erythematosus (also called SLE or lupus)
is an autoimmune condition. The normal role of your
body’s immune system is to fight off infections and
diseases to keep you healthy. In an autoimmune disease
like lupus, your immune system starts attacking your
own healthy tissues. For some people lupus may just
affect the skin and/or joints. In other people the lungs,
kidneys, blood vessels,
This document summarizes the mechanisms of systemic lupus erythematosus (SLE). It discusses genetic and environmental risk factors for SLE, including a stronger prevalence in females which implicates a role for sex hormones. It describes the diverse clinical presentations of SLE and important autoantibodies involved, such as anti-double stranded DNA antibodies. The document also discusses how these autoantibodies can cause tissue damage by binding to antigens in organs and activating the complement system, as seen in lupus nephritis. Overall, it provides an overview of the pathogenesis of SLE by involving genetic, environmental, and immunological factors.
"Gene Therapy" is a technique used to treat a disease or disorder by inducing the therapeutic gene into the vector, and the vector into the affected organism. So that, the therapeutic proteins expressed will vanish the affected proteins.
Introduction, causes and symptoms, Mechanism and treatment are been explained about this deadly disease SCID where production of T and B cells is affected.
Severe combined immunodeficiency (SCID) is a genetic disorder characterized by the absence of functional T lymphocytes and B lymphocytes, resulting in impaired adaptive immune system. There are several known types of SCID caused by mutations in different genes. The most common treatment is bone marrow transplantation, with success seen in transplants done in early infancy. Gene therapy is also being explored as a potential treatment through inserting missing genes into hematopoietic stem cells, though past trials increased leukemia risk and more research is still needed.
Contents- Introduction to Immunodeficiency | Types | SCID | LAD
Immunodeficiency is the inability to produce an adequate immune response because of insufficiency or absence of antibodies, immune cells or both.
SCID & LAD are the two immunodeficiencies from primary immunodeficiency.
The document discusses the importance of DNA replication for life and medicine. DNA replication is essential for cell division and is targeted by chemotherapy drugs to stop the growth of cancer cells. Understanding DNA replication better through research could help develop preventative treatments for diseases and improve medical knowledge.
This document summarizes the mechanisms of systemic lupus erythematosus (SLE). It discusses genetic and environmental risk factors for SLE, including a stronger prevalence in females which implicates a role for sex hormones. It describes the diverse clinical presentations of SLE and important autoantibodies involved, such as anti-double stranded DNA antibodies. The document also discusses how these autoantibodies can cause tissue damage by binding to antigens in organs and activating the complement system, as seen in lupus nephritis. Overall, it provides an overview of the pathogenesis of SLE by involving genetic, environmental, and immunological factors.
"Gene Therapy" is a technique used to treat a disease or disorder by inducing the therapeutic gene into the vector, and the vector into the affected organism. So that, the therapeutic proteins expressed will vanish the affected proteins.
Introduction, causes and symptoms, Mechanism and treatment are been explained about this deadly disease SCID where production of T and B cells is affected.
Severe combined immunodeficiency (SCID) is a genetic disorder characterized by the absence of functional T lymphocytes and B lymphocytes, resulting in impaired adaptive immune system. There are several known types of SCID caused by mutations in different genes. The most common treatment is bone marrow transplantation, with success seen in transplants done in early infancy. Gene therapy is also being explored as a potential treatment through inserting missing genes into hematopoietic stem cells, though past trials increased leukemia risk and more research is still needed.
Contents- Introduction to Immunodeficiency | Types | SCID | LAD
Immunodeficiency is the inability to produce an adequate immune response because of insufficiency or absence of antibodies, immune cells or both.
SCID & LAD are the two immunodeficiencies from primary immunodeficiency.
The document discusses the importance of DNA replication for life and medicine. DNA replication is essential for cell division and is targeted by chemotherapy drugs to stop the growth of cancer cells. Understanding DNA replication better through research could help develop preventative treatments for diseases and improve medical knowledge.
Dr. Ryan's Geriatric Immunology presentation from Badger Veterinary Hospital's Caring for Your Geriatric Horse February 13, 2013 client education seminar.
Diabetes Milletes involves the stimulation of beta-cell specific T cells by autoantigens like insulin, GAD, IA-2, and IGRP. This stimulation causes the production of T cells or autoantibodies that attack and destroy pancreatic beta cells. Genetics like AIRE and HLA genes as well as environmental factors like viruses can trigger this autoimmune response. While autoantibody tests can predict diabetes risk by detecting antibodies against islet cell antigens, no effective immunological interventions currently exist to prevent beta-cell destruction once the autoimmune process begins.
B-cell deficiency is a condition where the body has impaired humoral immunity due to a lack of proper B-cell function. B-cells play an important role in regulating the immune response, and dysregulation can lead to health issues. B-cell deficiency can be caused by not enough or non-functioning B-cells, plasma cells they differentiate into, or antibodies secreted by plasma cells. Symptoms include sinus infections, sepsis, skin infections, and pneumonia due to bacteria, fungi, viruses, and protozoa. Diagnosis involves measuring immunoglobulin levels and B-cell counts. Treatment focuses on managing infections, surveillance of potential malignancies, and immunoglobulin replacement therapy.
Gene therapy involves using genes to treat disease, such as cancer. It works by inserting a functional gene into a patient's cells to fight the disease. For cancer treatment, genes are inserted using an engineered adenovirus vector. One application is inserting the p53 tumor suppressor gene, which causes cancer cells to self-destruct. The document describes p53 gene therapy being administered directly into tumors or through injection for several cancer patients. Many showed tumor shrinkage or complete remission with only mild side effects like fever. Gene therapy is a promising treatment when combined with conventional therapies.
The document discusses the susceptibility of NC/Nga mice to Listeria monocytogenes (LM) infection compared to other mouse strains. Figure 2 shows that NC/Nga mice have decreasing levels of the protective cytokine IFN-γ and increasing levels of the anti-inflammatory cytokine IL-10 after LM infection. This suggests high IL-10 levels may explain the mice's susceptibility. However, Figures 3 and 4 appear to contradict this, so more research is needed to understand IL-10's role in listeriosis.
Autoimmunity and Susceptibility in WomenPriyaa1808
Women are more prone to developing autoimmune diseases than men. Several factors contribute to this predisposition in women, including hormonal differences. Estrogen is thought to enhance immune responses, leading to a more robust inflammatory response in women. Many autoimmune diseases are also associated with specific genetic factors, like certain HLA alleles, which can influence the development of autoimmunity. Environmental triggers, like infections, can also play a role through mechanisms like molecular mimicry, where foreign antigens resemble self-antigens and trigger an autoimmune response. Mouse models of human autoimmune diseases have provided insights into the genetic and pathological mechanisms involved.
This article analyzes the association between polymorphisms in the TNF-α and IFN-Y genes and the susceptibility and severity of systemic lupus erythematosus (SLE). The study found that SLE patients had significantly higher levels of TNF-α and IFN-Y in the plasma compared to healthy controls. Additionally, polymorphisms in the TNF-α and IFN-Y genes were detected and increased the susceptibility of individuals to acquire SLE, though they did not affect the severity of disease symptoms. There are factors like ethnic origin and genetic and epigenetic interactions that could produce changes in the results, and TNF-α and IFN-Y could be excellent pharmacological targets for SLE treatment.
Gene therapy is that the introduction of a traditional gene into an individual’s genome so as to repair a mutation that causes a genetic disorder.
When a traditional gene is inserted into a mutant nucleus, it presumably will integrate into a chromosomal site different from the defective allele; although this might repair the mutation, a replacement mutation may result if the traditional gene integrates into another functional gene.
Human gene therapy has been attempted only on somatic (body) cells for diseases like cancer and severe combined immunodeficiency syndrome (SCIDS).
This document outlines the history and mechanisms of the indoleamine-2,3-dioxygenase (IDO) pathway and its role in cancer immunotherapy. It discusses key findings such as:
1) Munn's 1999 discovery that IDO suppresses T-cell mediated rejection of tumors and fetal allografts by depleting tryptophan.
2) Mechanistic studies showing IDO induces T-cell arrest and inhibits proliferation through tryptophan depletion and kynurenine production, leading to Treg differentiation and CTL inhibition.
3) Preclinical studies combining IDO inhibitors with chemotherapy or vaccines, showing enhanced anti-tumor effects.
4) Ongoing clinical
This document summarizes combined immunodeficiency (CID), a disorder characterized by defects in the production or maturation of T cells and/or B cells, leaving the body without necessary immunity. There are two main types of CID - mutagenic defects due to genetic mutations and enzyme deficiencies from lack of enzymes. Mutagenic CIDs can be autosomal recessive or X-linked. Treatments discussed include bone marrow transplantation, gene therapy, passive antibody administration, and enzyme replacement.
Neutrophils play an important role in the early stages of Mycobacterial infection by recruiting to sites of infection and phagocytosing bacteria. However, their overall impact is complex, as they may both help control infection initially but also potentially disseminate bacteria as "Trojan horses" to other organs. While neutrophils have antimicrobial mechanisms, it is unclear if they can directly kill all Mycobacterial species. Their interactions with macrophages in clearance of apoptotic neutrophils and antigen presentation also influence acquired immunity. Overall, neutrophils act as a "double-edged sword" in the pathogenesis of Mycobacterial infections.
This document covers molecular genetics and genetic engineering, including DNA structure and replication, protein synthesis through transcription and translation, the genetic code, the human genome and its uses for diagnosis, therapy and research. It also discusses genetic engineering techniques like PCR and their uses in research, forensics and testing, as well as risks and applications in biotechnology for agriculture like GMOs and in biomedicine like gene therapy and production of human substances.
Severe combined immunodeficiency (SCID), also known as "bubble boy disease", is a genetic disorder where the immune system is impaired or absent. It affects both B cells and T cells. SCID can be diagnosed through newborn screening and symptoms include life-threatening infections in the first months of life. Treatment options include preventing infections, enzyme therapy for some types of SCID, gene therapy, and bone marrow transplantation which has been successful using matched or half-matched donors. The original "bubble boy" David Vetter died after transplantation due to an unscreened virus in his donor marrow.
This document discusses biosafety considerations for gene therapy. It provides an overview of criteria used to categorize biological risk and ensure appropriate containment procedures when working with vectors like adeno-associated virus (AAV). Gene therapy aims to treat diseases by gene replacement, correction, or silencing. Viral vectors are often used to deliver therapeutic genes and AAV is particularly promising due to its ability to infect cells and lack of pathogenicity. Risk assessment and containment procedures should match the assigned biosafety level of the agent being used.
HIV-1 Control: Exploiting the HERV-K102 - AFP Immunosenescence ParadigmDr. Marian Laderoute
1) The document discusses a new paradigm where immunosenescence (immune aging) involves blocked release of HERV-K102 particles from foamy macrophages due to increased levels of alpha-fetoprotein (AFP).
2) HERV-K102 is endogenously produced in response to HIV-1 and other infections but its release is inhibited in progressive cases, preventing its protective and virolytic effects.
3) The paradigm suggests exploiting HERV-K102 particle production or administration, combined with agents to reduce AFP levels, could provide functional cures or prevention for HIV-1 by activating autoimmunity against infected cells.
This document provides an overview of gene therapy and its applications in cancer, HIV/AIDS, and hereditary diseases. It discusses how gene therapy works by using vectors to deliver therapeutic genes into target cells to repair faulty genes. For cancer, strategies discussed include enhancing immune response, inserting suicide genes, and blocking oncogenes. For HIV/AIDS, intracellular immunization, ribozymes, transdominant mutants, and Trojan horses are described as strategies. For hereditary diseases, successes in clinical trials for SCID and hemophilia are summarized, with future trials planned for other genetic disorders.
severe combined immunodeficiency syndromeFatima Sayeed
Severe combined immunodeficiency syndrome (SCID) is a rare genetic disorder characterized by the absence of both T cells and B cells. This leaves the body unable to fight infections and affected infants often develop severe, life-threatening infections within the first year of life if untreated. There are 13 known genetic causes of SCID. The main treatment is a bone marrow transplant from a matched donor, which can cure the condition if performed early in life. Gene therapy is also being explored as a potential treatment.
Gene therapy refers to the insertion of genetic material to correct a genetic defect.
In gene therapy, a "normal" gene is inserted into the genome to replace an "abnormal," disease-causing gene
The document discusses gene therapy as a promising approach for treating various diseases. It provides a brief history of gene therapy and describes some of the early clinical trials. It then explains some of the key concepts in medical genetics like DNA, genes, and enzymes. Different methods for gene delivery are also summarized, including viral vectors, physical methods, and chemical methods. Applications of gene therapy for cancer, neurological disorders, and other diseases are briefly mentioned.
1) Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by unpredictable exacerbations and remissions affecting multiple organ systems.
2) The case report describes an 11-year old Indian boy who presented with fever and pancytopenia and was subsequently diagnosed with SLE based on rash, oral ulcers, arthritis, and strongly positive autoantibody tests.
3) He responded well to pulse steroids and IV immunoglobulin therapy and was put on long-term immunosuppressants for maintenance treatment.
The pathogenesis of NF1 is complex and involves interrelationships between various elements that manifest at different ages. Café-au-lait spots typically appear in the first year of life, while NF2 vestibular schwannomas usually develop later in the third decade. Symptoms of Schwannomatosis also appear later in life and are non-specific, like pain. Understanding how clinical signs relate to a person's age can help with healthcare and provide insights into pathogenesis. In some cases, genetic analysis may help with diagnosis when clinical symptoms are unclear. Somatic mosaicism can also contribute to limited signs and symptoms.
Dr. Ryan's Geriatric Immunology presentation from Badger Veterinary Hospital's Caring for Your Geriatric Horse February 13, 2013 client education seminar.
Diabetes Milletes involves the stimulation of beta-cell specific T cells by autoantigens like insulin, GAD, IA-2, and IGRP. This stimulation causes the production of T cells or autoantibodies that attack and destroy pancreatic beta cells. Genetics like AIRE and HLA genes as well as environmental factors like viruses can trigger this autoimmune response. While autoantibody tests can predict diabetes risk by detecting antibodies against islet cell antigens, no effective immunological interventions currently exist to prevent beta-cell destruction once the autoimmune process begins.
B-cell deficiency is a condition where the body has impaired humoral immunity due to a lack of proper B-cell function. B-cells play an important role in regulating the immune response, and dysregulation can lead to health issues. B-cell deficiency can be caused by not enough or non-functioning B-cells, plasma cells they differentiate into, or antibodies secreted by plasma cells. Symptoms include sinus infections, sepsis, skin infections, and pneumonia due to bacteria, fungi, viruses, and protozoa. Diagnosis involves measuring immunoglobulin levels and B-cell counts. Treatment focuses on managing infections, surveillance of potential malignancies, and immunoglobulin replacement therapy.
Gene therapy involves using genes to treat disease, such as cancer. It works by inserting a functional gene into a patient's cells to fight the disease. For cancer treatment, genes are inserted using an engineered adenovirus vector. One application is inserting the p53 tumor suppressor gene, which causes cancer cells to self-destruct. The document describes p53 gene therapy being administered directly into tumors or through injection for several cancer patients. Many showed tumor shrinkage or complete remission with only mild side effects like fever. Gene therapy is a promising treatment when combined with conventional therapies.
The document discusses the susceptibility of NC/Nga mice to Listeria monocytogenes (LM) infection compared to other mouse strains. Figure 2 shows that NC/Nga mice have decreasing levels of the protective cytokine IFN-γ and increasing levels of the anti-inflammatory cytokine IL-10 after LM infection. This suggests high IL-10 levels may explain the mice's susceptibility. However, Figures 3 and 4 appear to contradict this, so more research is needed to understand IL-10's role in listeriosis.
Autoimmunity and Susceptibility in WomenPriyaa1808
Women are more prone to developing autoimmune diseases than men. Several factors contribute to this predisposition in women, including hormonal differences. Estrogen is thought to enhance immune responses, leading to a more robust inflammatory response in women. Many autoimmune diseases are also associated with specific genetic factors, like certain HLA alleles, which can influence the development of autoimmunity. Environmental triggers, like infections, can also play a role through mechanisms like molecular mimicry, where foreign antigens resemble self-antigens and trigger an autoimmune response. Mouse models of human autoimmune diseases have provided insights into the genetic and pathological mechanisms involved.
This article analyzes the association between polymorphisms in the TNF-α and IFN-Y genes and the susceptibility and severity of systemic lupus erythematosus (SLE). The study found that SLE patients had significantly higher levels of TNF-α and IFN-Y in the plasma compared to healthy controls. Additionally, polymorphisms in the TNF-α and IFN-Y genes were detected and increased the susceptibility of individuals to acquire SLE, though they did not affect the severity of disease symptoms. There are factors like ethnic origin and genetic and epigenetic interactions that could produce changes in the results, and TNF-α and IFN-Y could be excellent pharmacological targets for SLE treatment.
Gene therapy is that the introduction of a traditional gene into an individual’s genome so as to repair a mutation that causes a genetic disorder.
When a traditional gene is inserted into a mutant nucleus, it presumably will integrate into a chromosomal site different from the defective allele; although this might repair the mutation, a replacement mutation may result if the traditional gene integrates into another functional gene.
Human gene therapy has been attempted only on somatic (body) cells for diseases like cancer and severe combined immunodeficiency syndrome (SCIDS).
This document outlines the history and mechanisms of the indoleamine-2,3-dioxygenase (IDO) pathway and its role in cancer immunotherapy. It discusses key findings such as:
1) Munn's 1999 discovery that IDO suppresses T-cell mediated rejection of tumors and fetal allografts by depleting tryptophan.
2) Mechanistic studies showing IDO induces T-cell arrest and inhibits proliferation through tryptophan depletion and kynurenine production, leading to Treg differentiation and CTL inhibition.
3) Preclinical studies combining IDO inhibitors with chemotherapy or vaccines, showing enhanced anti-tumor effects.
4) Ongoing clinical
This document summarizes combined immunodeficiency (CID), a disorder characterized by defects in the production or maturation of T cells and/or B cells, leaving the body without necessary immunity. There are two main types of CID - mutagenic defects due to genetic mutations and enzyme deficiencies from lack of enzymes. Mutagenic CIDs can be autosomal recessive or X-linked. Treatments discussed include bone marrow transplantation, gene therapy, passive antibody administration, and enzyme replacement.
Neutrophils play an important role in the early stages of Mycobacterial infection by recruiting to sites of infection and phagocytosing bacteria. However, their overall impact is complex, as they may both help control infection initially but also potentially disseminate bacteria as "Trojan horses" to other organs. While neutrophils have antimicrobial mechanisms, it is unclear if they can directly kill all Mycobacterial species. Their interactions with macrophages in clearance of apoptotic neutrophils and antigen presentation also influence acquired immunity. Overall, neutrophils act as a "double-edged sword" in the pathogenesis of Mycobacterial infections.
This document covers molecular genetics and genetic engineering, including DNA structure and replication, protein synthesis through transcription and translation, the genetic code, the human genome and its uses for diagnosis, therapy and research. It also discusses genetic engineering techniques like PCR and their uses in research, forensics and testing, as well as risks and applications in biotechnology for agriculture like GMOs and in biomedicine like gene therapy and production of human substances.
Severe combined immunodeficiency (SCID), also known as "bubble boy disease", is a genetic disorder where the immune system is impaired or absent. It affects both B cells and T cells. SCID can be diagnosed through newborn screening and symptoms include life-threatening infections in the first months of life. Treatment options include preventing infections, enzyme therapy for some types of SCID, gene therapy, and bone marrow transplantation which has been successful using matched or half-matched donors. The original "bubble boy" David Vetter died after transplantation due to an unscreened virus in his donor marrow.
This document discusses biosafety considerations for gene therapy. It provides an overview of criteria used to categorize biological risk and ensure appropriate containment procedures when working with vectors like adeno-associated virus (AAV). Gene therapy aims to treat diseases by gene replacement, correction, or silencing. Viral vectors are often used to deliver therapeutic genes and AAV is particularly promising due to its ability to infect cells and lack of pathogenicity. Risk assessment and containment procedures should match the assigned biosafety level of the agent being used.
HIV-1 Control: Exploiting the HERV-K102 - AFP Immunosenescence ParadigmDr. Marian Laderoute
1) The document discusses a new paradigm where immunosenescence (immune aging) involves blocked release of HERV-K102 particles from foamy macrophages due to increased levels of alpha-fetoprotein (AFP).
2) HERV-K102 is endogenously produced in response to HIV-1 and other infections but its release is inhibited in progressive cases, preventing its protective and virolytic effects.
3) The paradigm suggests exploiting HERV-K102 particle production or administration, combined with agents to reduce AFP levels, could provide functional cures or prevention for HIV-1 by activating autoimmunity against infected cells.
This document provides an overview of gene therapy and its applications in cancer, HIV/AIDS, and hereditary diseases. It discusses how gene therapy works by using vectors to deliver therapeutic genes into target cells to repair faulty genes. For cancer, strategies discussed include enhancing immune response, inserting suicide genes, and blocking oncogenes. For HIV/AIDS, intracellular immunization, ribozymes, transdominant mutants, and Trojan horses are described as strategies. For hereditary diseases, successes in clinical trials for SCID and hemophilia are summarized, with future trials planned for other genetic disorders.
severe combined immunodeficiency syndromeFatima Sayeed
Severe combined immunodeficiency syndrome (SCID) is a rare genetic disorder characterized by the absence of both T cells and B cells. This leaves the body unable to fight infections and affected infants often develop severe, life-threatening infections within the first year of life if untreated. There are 13 known genetic causes of SCID. The main treatment is a bone marrow transplant from a matched donor, which can cure the condition if performed early in life. Gene therapy is also being explored as a potential treatment.
Gene therapy refers to the insertion of genetic material to correct a genetic defect.
In gene therapy, a "normal" gene is inserted into the genome to replace an "abnormal," disease-causing gene
The document discusses gene therapy as a promising approach for treating various diseases. It provides a brief history of gene therapy and describes some of the early clinical trials. It then explains some of the key concepts in medical genetics like DNA, genes, and enzymes. Different methods for gene delivery are also summarized, including viral vectors, physical methods, and chemical methods. Applications of gene therapy for cancer, neurological disorders, and other diseases are briefly mentioned.
1) Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by unpredictable exacerbations and remissions affecting multiple organ systems.
2) The case report describes an 11-year old Indian boy who presented with fever and pancytopenia and was subsequently diagnosed with SLE based on rash, oral ulcers, arthritis, and strongly positive autoantibody tests.
3) He responded well to pulse steroids and IV immunoglobulin therapy and was put on long-term immunosuppressants for maintenance treatment.
The pathogenesis of NF1 is complex and involves interrelationships between various elements that manifest at different ages. Café-au-lait spots typically appear in the first year of life, while NF2 vestibular schwannomas usually develop later in the third decade. Symptoms of Schwannomatosis also appear later in life and are non-specific, like pain. Understanding how clinical signs relate to a person's age can help with healthcare and provide insights into pathogenesis. In some cases, genetic analysis may help with diagnosis when clinical symptoms are unclear. Somatic mosaicism can also contribute to limited signs and symptoms.
CAR-T cells are genetically modified T cells that are designed to target and destroy cancer cells. They contain chimeric antigen receptors (CARs) that allow them to recognize specific antigens on tumor cells independently of the normal T cell receptor. The CAR is composed of an extracellular antigen recognition domain attached to transmembrane and co-stimulatory domains, allowing the modified T cells to directly bind and kill cancer cells upon antigen recognition and initiate an immune response against the tumor.
Systemic lupus erythematosus (SLE) is an autoimmune disease where organs and cells are damaged by autoantibodies and immune complexes. It predominantly affects women aged 15-45 and can involve any organ. Renal involvement, known as lupus nephritis, ranges from mild mesangial proliferation to severe necrotizing glomerulonephritis. A renal biopsy is needed to classify lupus nephritis based on immune deposits and patterns of injury, which guides treatment and prognosis.
This document examines the encephalogenic and HLA-DR binding capacities of various myelin peptides. It constructs recombinant HLA-DRβ1 complexes containing peptides from myelin proteolipid protein, myelin oligodendrocyte glycoprotein, and myelin basic protein. These complexes are transfected into insect cells to evaluate surface expression and autoantigenic activity. Individual myelin peptides are also tested for their ability to induce experimental autoimmune encephalomyelitis in transgenic mice. The data shows that two specific sheath peptides induced multiple sclerosis-like paralysis when injected into HLA-DRβ1-15.01 mice, indicating a role in multiple sclerosis induction. Ultimately, the peptide-HLA complexes will be used
The document discusses various hypotheses for the pathogenesis of paraneoplastic syndromes. It is now accepted that paraneoplastic syndromes are immune-mediated disorders triggered when a tumor expresses neural antigens, leading the immune system to attack both the cancer and nervous system. However, questions remain regarding the specific immune mechanisms and why some tumors are destroyed while others persist and prove lethal.
Tuberculosis is a lung disease caused by the bacterium Mycobacterium tuberculosis. It remains a major global health problem. In 2020, there were an estimated 10 million new TB cases and 1.5 million TB deaths worldwide, making it one of the top 10 causes of death globally. The disease disproportionately affects low and middle income countries. Key risk factors include poverty, HIV infection and indoor air pollution. Early diagnosis and complete treatment are important for controlling the spread of the disease.
Apoptosis, or programmed cell death, plays an important role in development, immunity, and maintenance of genomic integrity. Disruption of apoptosis can lead to diseases like cancer, autoimmune disorders, and neurodegenerative diseases. The document discusses the key stages and molecular mechanisms of apoptosis, including the roles of caspases, Bcl-2 family proteins, and death receptors. It also covers the importance of apoptosis in processes like immune system development, tissue remodeling, and response to DNA damage. Therapeutic strategies aim to either inhibit inappropriate apoptosis or induce apoptosis in conditions like cancer.
Stem cells, particularly autologous stem cells extracted from a patient's own bone marrow, show promise in treating multiple sclerosis (MS). Studies have found autologous stem cell transplantation after immunosuppression can reduce progression of MS, especially for patients with relapsing-remitting MS rather than primary progressive MS. While stem cells may not cure MS completely, they can help regenerate myelin sheaths and slow the degenerative effects of the disease on the nervous system. More research is still needed but stem cell therapy offers new opportunities for delivering high doses of immunosuppression to potentially stop MS progression.
Neutrophils are the most abundant white blood cells, accounting for up to 70% of circulating leukocytes. They are produced in high numbers in the bone marrow to act as sentinels of the innate immune system. Neutrophils have a short lifespan of 10 hours in circulation and up to 48 hours in tissues. They are recruited from blood vessels to sites of infection or damage, where they engulf and kill microbes using oxidative and non-oxidative mechanisms. Neutrophils also release neutrophil extracellular traps that ensnare bacteria. While defending against pathogens, neutrophils must be cleared from tissues to resolve inflammation and prevent tissue damage from their antimicrobial enzymes.
Behavioral immunology ( Behavioral immunology” refers to the branch of behavioral medicine concerned with bidirectional interactions between behavior and the immune system).
The document discusses behavioral immunology and the bidirectional relationship between behavior and the immune system. It provides examples of how the immune system interacts with behavior in swordfish, electric eels, and sex differences in immune response. The thymus is described as an organ that helps develop T-cells. The behavioral immune system can influence prejudices and disease avoidance behaviors in humans.
Natural killer (NK) cells are a type of lymphocyte that plays a major role in the innate immune system by killing tumor cells and virally infected cells. NK cells are cytotoxic and contain granules with proteins like perforin and granzymes that can induce apoptosis in target cells. Patients deficient in NK cells are highly susceptible to herpes virus infections. NK cells recognize and kill tumor or infected cells but can also communicate signals to block destruction of tumors or viruses depending on the signals they receive. They are activated through killer activating receptors. [END SUMMARY]
This document provides an overview of systemic lupus erythematosus (SLE), an autoimmune disease where the immune system attacks healthy tissue. It discusses the causes, signs and symptoms, immunological findings, diagnosis and pathophysiology of SLE. Key points include that SLE affects many organs but most often harms the heart, joints, skin, lungs, kidneys and blood vessels; common symptoms are fatigue, rashes and joint pain; diagnosis involves testing for antinuclear antibodies and antibodies to double-stranded DNA, histones and other nuclear antigens; and the disease is thought to be caused by a combination of genetic and environmental factors impacting apoptosis and clearance of cellular debris.
My son had Wiskott Aldrich Syndrome (WAS). He had a bone marrow transplant in August 2006. His WAS is healed. This presentation was designed by some grad students. Some of the content is from my blog and it pictures my son, David. http://www.davidmcnally.blogspot.com
This document describes the rare case of a 59-year-old male patient who received the first kidney transplant (KTx) in India in 1959. He underwent a living unrelated donor kidney transplant and splenectomy. He was treated with azathioprine and prednisone for immunosuppression. In 2002 he experienced chronic rejection but recovered well after treatment. He continued on standard immunosuppression treatment and remained alive for over 15 years after his transplant despite developing complications like post-transplant diabetes mellitus, which was managed with insulin. This was one of the earliest reported cases of kidney transplantation in India.
Vesicoureteral reflux is a condition where urine flows back from the bladder into the ureters and kidneys. It can cause kidney infections and scarring. There are two types - primary reflux where the lower urinary tract functions normally, and secondary reflux associated with obstruction. Reflux is diagnosed using voiding cystourethrogram and renal ultrasound. Treatment involves antibiotics to prevent infections, sometimes long-term antibiotic prophylaxis, and surgery to correct high-grade reflux. Medical management is initially tried in most cases as reflux often resolves spontaneously with time.
This document discusses a case of malignant lymphoma in a patient presenting with fever, cough, dyspnea and sweating. Investigations revealed anemia, elevated white blood cell count, and a pleural fluid analysis showing yellow, turbid fluid with a high cell count and atypical cells. A biopsy confirmed the presence of malignant lymphocytes, leading to a diagnosis of malignant lymphoma. The document then discusses staging, types, treatment and prognosis of malignant lymphoma.
This document describes Gloriosa superba poisoning from ingestion of the plant's tubers. It provides details on the patient's presentation, clinical course, toxic effects on organ systems, and management recommendations. Key points include severe gastroenteritis, hypotension, renal failure, bone marrow suppression, and potential death from shock or respiratory failure. Decontamination, fluid/electrolyte replacement, ventilation support, and monitoring for complications are advised. No antidote exists though immunotherapy is being studied.
TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kol...rightmanforbloodline
TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kolb, Ian Q. Whishaw, Verified Chapters 1 - 16, Complete Newest Versio
TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kolb, Ian Q. Whishaw, Verified Chapters 1 - 16, Complete Newest Version
TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kolb, Ian Q. Whishaw, Verified Chapters 1 - 16, Complete Newest Version
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
Promoting Wellbeing - Applied Social Psychology - Psychology SuperNotesPsychoTech Services
A proprietary approach developed by bringing together the best of learning theories from Psychology, design principles from the world of visualization, and pedagogical methods from over a decade of training experience, that enables you to: Learn better, faster!
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
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These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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In some case, your chronic prostatitis may be related to over-masturbation. Generally, natural medicine Diuretic and Anti-inflammatory Pill can help mee get a cure.
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Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
3. Introduction A “Lady” between Spiderman and superman, that is Systemic Lupus Erythematosis (SLE) is a chronic inflammatory state that we encounter every day
7. Lupus Wolf mutilates it’s pray before it eats without killing, in the similar way the SLE does. Ref:. Graves, Will (2007). Wolves in Russia: Anxiety throughout the ages. DetseligEnterprises.ISBN 1550593323 “They kill large prey by biting large chunks of flesh from the soft perineum area, causing massive blood loss. Such bites can cause wounds 10–15 cm in length, with three such bites to the perineum usually being sufficient to bring down a large deer in optimum health”
8. SLE second most common human autoimmune disease in the world. Ref: Can morbidity and mortality of SLE be improved? Anurekha Bongu Elizabeth Chang Rosalind Ramsey-Goldman Best Practice & Research Clinical RheumatologyVolume 16, Issue 2,April 2002, Pages 313-332 Northwestern University Medical School, ArthritisChicago Ave, Chicago, IL, 60611, USA. Available online 10 June 2002.
9. SLE SLE is the second most common autoimmune disorder (after thyroid disease) in women of childbearing age. Lupus is increasingly being recognized throughout the world's population. The incidence and prevalence of SLE varies among racial and ethnic groups. Lupus patient survival has significantly improved over the past five decades, but a three- to fivefold increased risk of death remains compared with the general population. As lupus patients survive longer, these individuals face a range of complications from the disease itself or consequent to its treatment. Emerging data from epidemiological studies underscore the importance of incorporating race and ethnicity in understanding the risk factors leading to the significant burden of mortality and morbidity associated with this disease; Anurekha Bongu Elizabeth
10. Prevalence of SLE India A point prevalence of 3.2 per 100 000 (95% CI = 0-6.86 per 100 000). Ref:Prevalence of Systemic Lupus Erythematosus in India(North)A.N. Malaviyadoi: 10.1177/096120339300200209. Lupus April 1993 vol. 2 no. 2 115-118
11. INDIA - FEMALE Majority of the sufferers are females of the menstruating period. It affects predominantly women in their reproductive years. The median age of onset in Indian SLE is 24.5 years and the sex ratio (F:M) is 11:1 Ref: A Kumar J: INDIAN GUIDELINES ON THE MANAGEMENT OF SLE. Indian Rheumatol Assoc 2002 : 10 : 80 - 96
12. We are still in the dark to find out a cause for this illness but we know that it is an autoimmune disease. Large number of drugs that fight against the illness was already there in the armamentarium and more in the pipe line.
13. But alas! Nothing found to be use full for the majority of SLE patients Who’s destiny is to land in the dialysis room or Kidney transplant arena with end stage Kidney failure and Those who escaped from suffering by reaching at the graveyards in the young age.
14. Americans Autoimmune diseases are common. Aaffecting > 23.5 million Americans. A Leading cause of death and disability
15. Unfortunate? Unable to cut short Treatment cost Sufferings Morbidity Mortality Their future is bleak.
16. Some rays of hope Lande, Christian Goosmann, and various others Unveiling of the pathologic Cellular mechanism of the autoimmunity Ref: 1. Roberto Lande, et al.Peptide Complexes in Systemic Lupus ErythematosusNeutrophils Activate PlasmacytoidDendritic Cells by Releasing Self-DNA.SciTransl Med 3, 73ra19 (2011 2. Volker Brinkmann, Britta Laube, Ulrike Abu Abed, Christian Goosmann, Arturo Zychlinsky.Neutrophil Extracellular Traps: How to Generate and Visualize Them. www.youtube.com/poyilil . Video Article 3.M. J. Shlomchik, Activating systemic autoimmunity: B’s, T’s, and tolls. Curr. Opin. Immunol.21, 626–633 (2009).
17. Autoimmunity By the breakdown of tolerance to nuclear self-antigens, which leads to activation of autoreactiveBcells that produce utoantibodies against self-nucleic acids and associated proteins.
18. Autoimmunity in SLE Results from hyper reactive B cells which initiate the T Helper/ suppressor deregulation results in the release of neutrophils characterized by chronic activation of plasmacytoid Dendritic Cells (pDCs) and production of autoantibodies against nuclear self-antigens. Ref: L. Rönnblom, V. Pascual, The innate immune system in SLE: Type I interferons and dendritic cells. Lupus 17, 394–399 (2008).
19. Organ specific expressions These autoantibodies bind self-nucleic acids released by dying cells, and form immune complexes that are deposited in different parts of the body, leading to detrimental inflammation and tissue damage.
20. Expressions of basic defects This results in various autoantibody production and deposition of immune complex in various organs.
21.
22. Early event that triggers autoimmunity A key early event that triggers autoimmunity in SLE is the chronic innate activation of pDCs to secrete type I interferons (IFNs).
23. IFNs The high levels of IFNs induce an unabated differentiation of monocytes into Dendritic cells that stimulate autoreactive B and T cells, and lower the activation threshold of autoreactive B cells, thereby promoting autoimmunity in SLE. Ref: A. N. Theofilopoulos, R. Baccala, B. Beutler, D. H. Kono, Type I interferons (a/b) in immunity and autoimmunity. Annu. Rev. Immunol. 23, 307–336 (2005). M. J. Shlomchik, Activating systemic autoimmunity: B’s, T’s, and tolls. Curr. Opin. Immunol.21, 626–633 (2009).
27. NET formation These immunogenic complexes composed of neutrophil-derived antimicrobial peptides and self-DNA. These complexes were produced by activated neutrophils in the form of web-like structures known as Neutrophil Extracellular Traps (NETs) and
31. Toll-like receptor 9 Efficiently triggered innate pDC activation via Toll-like receptor 9 (TLR9) Ref: Toll-like receptors in systemic autoimmune disease. A. Marshak-Rothstein, Nat. Rev. Immunol.6, 823–835 (2006).
32. 1. Mechanisms for type I interferon induction in TLR7/9-stimulated dendritic cells DCs sense nucleic acid adjuvants and produce type I interferon (IFN) in a subset-dependent manner. Among nucleic acid sensors, TLR7 and TLR9 are peculiar in that they recognize not only pathogen- but also host-derived nucleic acids. In fact, accumulating evidences suggest that TLR7/9-induced type I IFN production play important roles in pathogenesis of autoimmune disorders such as SLE. Therefore, clarifying the TLR7/9 signaling mechanisms should contribute to the development of therapeutic manipulation for such diseases.
36. Vicious cycle SLE patients were found to develop autoantibodies to both the self-DNA and antimicrobial peptides in NETs, indicating that these complexes could also serve as autoantigens to trigger B cell activation. Circulating neutrophils from SLE patients released more NETs than those from healthy donors.
37. VC This catches the antimicrobial autoantibodies and chronic release of immunogenic complexes in SLE making a vicious cycle.
39. W-A-S-P This establish a link between cells, neutrophils, pDC activation, and autoimmunity in SLE, providing new potential targets for the treatment of this devastating disease. Even though the research thinks that the B cell defect is due to the genetic predilection of the individuals.
40. Spiderman There is some way to prevent the proliferation and multiplication of B-cells are prevented, we can control SLE and other auto immune disease to certain extend. The NET produced by neutrophils are like the Spiderman’s net.
42. CELL DEATH There are two ways of cell death either by necrosis or by apoptotic. In case of necrotic or inflammatory cell death various cell debris like DNA, nucleolus, chromatids etc are released in to the extracellular space which normally cached in the NET and removed from the tissues.
44. APOPTOSIS Similarly apoptosis the cell debris are removed with out any immunological reactions. Ref:Hallmarksof the apoptotic and necrotic cell death process.(Pic)Apoptosis includes cellular shrinking, chromatin condensation and margination at the nuclear periphery with the eventual formation of membrane-bound apoptotic bodies that contain organelles, cytosol and nuclear fragments and are phagocytosed without triggering inflammatory processes.The necrotic cell swells, becomes leaky and finally is disrupted and releases its contents into the surrounding tissue resulting in inflammation. Modified from [Van Cruchten, 2002].
46. Spiderman Thus playing a wonderful role by the NET (Spiderman). In the case of autoimmune diseases and SLE either the apoptosis is defective or after apoptotic cell death the removal of the debris are defective.
48. NETOSIS It is proved that self-DNA in immune complexes of SLE patients contains Neutrophil antimicrobial peptide LL37 and HNP. These antimicrobial peptides were required for self-DNA to trigger TLR9 in pDCs by forming complexes with the DNA that is protected from extracellular degradation. Such immunogenic self-DNA–antimicrobial peptide complexes were released by dying neutrophils undergoing NETosis, a cell death process in which activated neutrophils extrude large amounts of nuclear DNA into the extracellular space in the form of web-like structures called NETs 8,9,10.
49. Net &Neutrophil NETs were abundantly released by neutrophils of SLE patients and were found to directly activate pDC to produce IFN-a. SLE patients developed autoantibodies to both the DNA and the antimicrobial peptides present in NETs, suggesting that NETs also trigger activation of autoreactive B cells.
50. CLINICAL IMPLICATIONS OF BASIC RESEARCH Thus, we@identify the ability of neutrophils to activate pDCs through the release of NETs and suggest that a dysregulation of this pathway drives chronic pDC activation and autoimmunity in SLE. Recent studies, such as those by Lande et al.@ and Garcia-Romo et al., have pushed the neutrophil to the forefront of the pathogenesis of SLE and have provided insight into how the implicated biochemical and cellular events are linked. Ref: CLINICAL IMPLICATIONS OF BASIC RESEARCH Systemic Lupus Erythematosus and the Neutrophil Xavier Bosch, M.D., Ph.D. N Engl J Med 2011; 365:758-760August 25, 2011
52. Clinical<Failure> Basic Once we failed to prevent the formation autoantibodies by the NET search continued to produce biologics (Superman) against the antibodies produced by the SLE. One antibody fails try another it fails try another.....
53. In pockets and pipeline Autoantibodiesseen in systemic lupus are directed against nuclear antigens such as nucleosomes, DNA, and histone proteins found within the body's cells and plasma. Autoantibodies are involved in disease development either by forming immune complexes that lodge in target organs, disrupting normal organ function, or by cross-reacting with targeted antigens and damaging tissue.
54. antibody Targets of autoantibodies in SLE include nuclear and cytoplasmic macromolecules, lipid components, and plasma proteins. The most frequently associated autoantibodies in SLE include smith (Sm), nucleosomes, histones, and double stranded (ds) DNA. Anti-dsDNA antibodies are the most frequently detected antibodies in SLE. Aberrancy in multiple components of the immune system including B cells, T cells, cytokines and growth factors.
55. Try try and try CD20 antibody. Rituximab, in SLE, reported an unexpected negative results. Belimumab, the monoclonal antibody against B-lymphocyte stimulator (BLyS), showed significant clinical benefit. Studies of a co-stimulation blocker (abatacept), tumor necrosis factor inhibitor (infliximab), and interleukin-6 inhibitor (tocilizumab) were either negative Studies of T cell and interferon inhibition remain in the early development phase.
56. TOMORROW? Excessive B cell function including autoantibody production is a common feature of SLE and considered to be intimately associated with spontaneous lymphokine secretion by themselves. To clarify roles of IL- 6/IL-6 receptor autocrine activation pathway in autoantibody production observed in patients with SLE, studied expression and function of IL- 6 receptors in comparison with those of IL-2 receptors, Tac on SLE B cells. IL-6 receptors and IL-2 receptors have been detected on B cells in the blood without any in vitro stimuli in most patients with SLE.
57. In pipeline The introduction of anti-IL-6 receptor antibody, which inhibits binding to the receptors of IL-6, and anti-IL-2 receptor antibody, anti-Tac to the cultures of SLE B cells resulted in potent inhibition of spontaneous production of polyclonal Ig and anti-DNA autoantibodies. In addition, fresh SLE B cells secreted high levels of IL-6 without any in vitro stimuli.
58. B cells the culprit? These results indicate that constitutive expression of IL-6 receptors on B cells in conjunction with spontaneous IL-6 production by B cells induces autocrine B cell activation, which may lead to B cell hyperactivity and autoantibody secretion in SLE patients.
59. Future Dysregulation of B cell activity observed in patients with SLE could thus be, at least in part, independent of T cell help. Several new targeted biologic agents for treating lupus nephritis are on the horizon; however, it is important to determine the circumstances in which they should be used, and how to optimally combine these agents with current or other new therapies.
60. hope@ Among the important ones are Tocilizumab a humanised monoclonal antibody that binds interleukin -6 (IL-6) receptors. Ustekunumabis a human immunoglobulin (Ig) G1 antibody that neutralizes IL-12 and IL-23 mediated common response.
61. Fusion proteins* Alefacept a Fusion protein of the CD-2 blinding region of leukocyte function associated antigen -3 and the CH2 and CH3 domain lgG1 inhibit T-cells activation and induces apoptosis of memory T-cells. Abataceptmodulates CD 80/CD86: CD28 Co-stimulatory signal needed for activation of T-cells.
62. Anakinra Anakinra competitively inhibit IL-1 binding to IL-1 type -1 receptor Retuximab. CD 20 directed cytotoxicantibody. Ref:Joanna m. Do biologics cause cancer? University of Michigan.17.08.2011.www.medscape.com.
64. The war and warriors The presence of NET (Spider web like) in the extra cellular space which (The Spiderman helps in the elimination of enemy ) get neutralized by some weapons (Neutrophil antimicrobial peptide LL37 and HNP) produced by the enemy in SLE.
65. Futile Attempts- Nepotism? The futile attempt in search of various biosimilars (Superman) to protect from SLE still continued.
67. REFERENCES 1. Roberto Lande, et al.Peptide Complexes in Systemic Lupus Erythematosus Neutrophils Activate Plasmacytoid Dendritic Cells by Releasing Self-DNA.SciTransl Med 3, 73ra19 (2011 2. Volker Brinkmann, Britta Laube, Ulrike Abu Abed, Christian Goosmann, Arturo Zychlinsky.Neutrophil Extracellular Traps: How to Generate and Visualize Them. www.youtube.com/poyilil. Video Article 3.M. J. Shlomchik, Activating systemic autoimmunity: B’s, T’s, and tolls. Curr. Opin. Immunol.21, 626–633 (2009). 4. L. Rönnblom, V. Pascual, The innate immune system in SLE: Type I interferons and dendritic cells. Lupus 17, 394–399 (2008). 5. A. N. Theofilopoulos, R. Baccala, B. Beutler, D. H. Kono, Type I interferons (a/b) in immunityand autoimmunity. Annu. Rev. Immunol. 23, 307–336 (2005).
68. 6. M. J. Shlomchik, Activating systemic autoimmunity: B’s, T’s, and tolls. Curr. Opin. Immunol.21, 626–633 (2009). 7. Toll-like receptors in systemic autoimmune disease. A. Marshak-Rothstein, Nat. Rev. Immunol.6, 823–835 (2006). 8. V. Brinkmann, U. Reichard, C. Goosmann, B. Fauler, Y. Uhlemann, D. S. Weiss, Y. Weinrauch, A. Zychlinsky, Neutrophil extracellular traps kill bacteria. Science 303, 1532–1535 (2004).
69. 9. T. A. Fuchs, U. Abed, C. Goosmann, R. Hurwitz, I. Schulze, V. Wahn, Y. Weinrauch, V. Brinkmann, A. Zychlinsky, Novel cell death program leads to neutrophil extracellular traps. J. Cell Biol. 176, 231–241 (2007). 10. V. Brinkmann, A. Zychlinsky, Beneficial suicide: Why neutrophils die to make NETs. Nat. Rev. Microbiol. 5, 577–582 (2007). 11. Joanna m. Do biologics cause cancer? University of Michigan.17.08.2011.www.medscape.com.