In immunology, autoimmunity is the system of immune responses of an organism against its own healthy cells, tissues and other normal body constituents. Any disease resulting from this type of immune response is termed an "autoimmune disease". Prominent examples include celiac disease, post-infectious IBS, diabetes mellitus type 1, Henoch–Schönlein purpura (HSP) sarcoidosis, systemic lupus erythematosus (SLE), Sjögren syndrome, eosinophilic granulomatosis with polyangiitis, Hashimoto's thyroiditis, Graves' disease, idiopathic thrombocytopenic purpura, Addison's disease, rheumatoid arthritis (RA), ankylosing spondylitis, polymyositis (PM), dermatomyositis (DM), and multiple sclerosis (MS). Autoimmune diseases are very often treated with steroids.
Antinuclear antibodies are autoantibodies that bind to contents of the cell nucleus. In normal individuals, the immune system produces antibodies to foreign proteins (antigens) but not to human proteins (autoantigens). In some cases, antibodies to human antigens are produced.
The National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) is one of the institutes and centers that make up the National Institutes of Health, an agency of the United States Department of Health and Human Services (HHS).
Immunodeficiency, also known as immunocompromisation, is a state in which the immune system's ability to fight infectious diseases and cancer is compromised or entirely absent. Most cases are acquired ("secondary") due to extrinsic factors that affect the patient's immune system. Examples of these extrinsic factors include HIV infection and environmental factors, such as nutrition. Immunocompromisation may also be due to genetic diseases/flaws such as SCID.
Molecular mimicry is defined as the theoretical possibility that sequence similarities between foreign and self-peptides are sufficient to result in the cross-activation of autoreactive T or B cells by pathogen-derived peptides. Despite the prevalence of several peptide sequences which can be both foreign and self in nature, a single antibody or TCR can be activated by just a few crucial residues which stresses the importance of structural homology in the theory of molecular mimicry. Upon the activation of B or T cells, it is believed that these "peptide mimic" specific T or B cells can cross-react with self-epitopes, thus leading to tissue pathology (autoimmunity). Molecular mimicry is a phenomenon that has been just recently discovered as one of several ways in which autoimmunity can be evoked. A molecular mimicking event is, however, more than an epiphenomenon despite its low statistical probability of occurring and these events have serious implications in the onset of many human autoimmune disorders.
Self-protein refers to all proteins endogenously produced by DNA-level transcription and translation within an organism of interest. This does not include proteins synthesized due to viral infection, but may include those synthesized by commensal bacteria within the intestines. Proteins that are not created within the body of the organism of interest, but nevertheless enter through the bloodstream, a breach in the skin, or a mucous membrane, may be designated as “non-self” and subsequently targeted and attacked by the immune system. Tolerance to self-protein is crucial for overall wellbeing; when the body erroneously identifies self-proteins as “non-self”, the subsequent immune response against endogenous proteins may lead to the development of an autoimmune disease.
B-cell activating factor (BAFF) also known as tumor necrosis factor ligand superfamily member 13B and CD257 among other names, is a protein that in humans is encoded by the TNFSF13B gene. BAFF is also known as B Lymphocyte Stimulator (BLyS) and TNF- and APOL-related leukocyte expressed ligand (TALL-1) and the Dendritic cell-derived TNF-like molecule.
Signal transducer and activator of transcription 4 (STAT4) is a transcription factor belonging to the STAT protein family, composed of STAT1, STAT2, STAT3, STAT4, STAT5A, STAT5B, STAT6. STAT proteins are key activators of gene transcription which bind to DNA in response to cytokine gradient. STAT proteins are a common part of Janus kinase (JAK)- signalling pathways, activated by cytokines.STAT4 is required for the development of Th1 cells from naive CD4+ T cells and IFN-γ production in response to IL-12. There are two known STAT4 transcripts, STAT4α and STAT4β, differing in the levels of interferon-gamma production downstream.
Certain sites of the mammalian body have immune privilege, meaning they are able to tolerate the introduction of antigens without eliciting an inflammatory immune response. Tissue grafts are normally recognised as foreign antigens by the body and attacked by the immune system. However, in immune privileged sites, tissue grafts can survive for extended periods of time without rejection occurring. Immunologically privileged sites include:
Interferon alpha-1 is a protein that in humans is encoded by the IFNA1 gene.
In immunology, clonal deletion is the removal through apoptosis of B cells and T cells that have expressed receptors for self before developing into fully immunocompetent lymphocytes. This prevents recognition and destruction of self host cells, making it a type of negative selection or central tolerance. Central tolerance prevents B and T lymphocytes from reacting to self. Thus, clonal deletion can help protect individuals against autoimmunity. Clonal deletion is thought to be the most common type of negative selection. It is one method of immune tolerance.
An autoimmune disease is a condition that results from an anomalous response of the immune system, wherein it mistakenly targets and attacks healthy, functioning parts of the body as if they were foreign organisms. It is estimated that there are more than 80 recognized autoimmune diseases, with recent scientific evidence suggesting the existence of potentially more than 100 distinct conditions. Nearly any body part can be involved.
Autoimmune polyendocrine syndrome type 1 (APS-1), is a subtype of autoimmune polyendocrine syndrome. It causes the dysfunction of multiple endocrine glands due to autoimmunity. It is a genetic disorder, inherited in autosomal recessive fashion due to a defect in the AIRE gene , which is located on chromosome 21 and normally confers immune tolerance.
Paolo Casali is an Italian-American immunologist. He is the Zachry Foundation Distinguished Professor at the Long School of Medicine of the University of Texas Health Science Center at San Antonio, and chairman of its department of microbiology, immunology and molecular genetics.
Robert George Lahita is an American physician, internist and rheumatologist, best known for his research into systemic lupus erythematosus. and other autoimmune diseases. He is the author of more than 16 books and 150 scientific publications in the field of autoimmunity and immuno-endocrinology and a media consultant on health-related issues. He currently serves as Director of the Institute of Autoimmune and Rheumatic Diseases at St. Joseph's Healthcare System, specializing in autoimmunity, rheumatology, and treatment of diseases of joints, muscle, bones and tendons including arthritis, back pain, muscle strains, common athletic injuries and collagen diseases.
Dipyaman Ganguly is an Indian physician-scientist immunologist and cell biologist, currently a Principal Scientist and Swarnajayanthi Fellow at the CSIR-Indian Institute of Chemical Biology (IICB). He heads the Dendritic Cell Laboratory of IICB, popularly known as Ganguly Lab, where he hosts several researchers involved in research on regulation of innate Immunity and pathogenesis of inflammatory disorders.
Noel R. Rose, was an American immunologist, pathologist, and molecular microbiologist. He is widely known for pioneering autoimmunity during the 1950s and made several contributions to the field of autoimmunity, which brought in the modern era of research into autoimmune disease. He is often referred to as the "Father of Autoimmunity".
Silvia Bolland is an American biomedical scientist serving as chief of the autoimmunity and functional genomics section at the National Institute of Allergy and Infectious Diseases.
Fabienne Mackay is a French Australian research immunologist and institutional leader within the Australian medical research, education and innovation sectors. She is the Director and CEO of the QIMR Berghofer Medical Research Institute since 2020, after being the inaugural Head of the School of Biomedical Sciences at the University of Melbourne during the preceding five years. She is also an Honorary Professor at the Faculties of Medicine of the University of Queensland and the University of Melbourne. Her work has attracted public attention for its contribution to the pathophysiological understanding and treatment of lupus and other autoimmune diseases. Mackay has been notably awarded, achieving international reputation for her widely cited research describing B-cell activating factor (BAFF) and other cytokines of the TNF receptor superfamily, and their roles in B cell physiology, autoimmunity and cancer. She is an elected Fellow of the Australian Academy of Health and Medical Sciences.
