What Are Some Examples Of Autoimmune Diseases – In immunology, autoimmunity is the body’s immune response to its own healthy cells, tissues, and other normal bodies.
Any disease that results from this type of immune response is called an “autoimmune disease.” Notable examples include celiac disease, post-infectious IBS, type 1 diabetes, sarcoidosis, Hoch-Schonlein purpura (HSP), systemic lupus erythematosus (SLE), Sjogr syndrome, eosinophilic granulomatosis with polyangiitis, Hashimoto’s purpura, thyroid gravid. , Addison’s disease, rheumatoid arthritis (RA), ankylosing spondylitis, polymyositis (PM), dermatomyositis (DM), alopecia areata
What Are Some Examples Of Autoimmune Diseases
Autoimmunity refers to the appearance of antibodies or T cells that react with one’s own proteins and is prevalent in all persons with normal health. It causes autoimmune diseases, where autoreactivity can cause tissue damage.
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At the end of the 20th century, it was believed that the immune system could not react to the body’s own tissues. Paul Ehrlich proposed the concept of autotoxic horror at the end of the 20th century. Ehrlich later adapted his theory to recognize the possibility of autoimmune tissue attack, but he believed that some innate protective mechanisms would prevent the autoimmune response from becoming pathological.
In 1904, this theory was challenged when a substance that reacted with red blood cells was found in the serum of patients with paroxysmal cold hemoglobinuria. Over the next few decades, several conditions could be linked to autoimmune responses. However, the authoritative status of Ehrlich’s postulate hindered the understanding of these findings. Immunology has become a biochemical rather than a clinical discipline.
More precisely, autoimmune responses are known to be an integral part of the vertebrate immune system (sometimes called “natural autoimmunity”).
While high levels of autoimmunity are unhealthy, low levels of autoimmunity can actually be beneficial. Taking further experience of the good factor of autoimmunity, one could assume that autoimmunity is always a self-defense mechanism of the mammalian system for survival. The system does not randomly lose the ability to distinguish between self and non-self; the attack on the cells may be the result of a cycle of metabolic processes necessary to maintain the homeostasis of blood chemistry.
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Second, autoimmunity may play a role in facilitating a rapid immune response in the early stages of infection, when the availability of foreign antibodies limits the response (ie, when pathogens are scarce). In their study, Stefanova et al. (2002) injected an MHC class II antibody into mice expressing only one type of MHC class II molecule (H-2).
) to temporarily prevent CD4+ T cell-MHC interaction. Naïve CD4+ T cells (not prechallenged with non-self antigens) recovered from these mice 36 h after anti-MHC administration showed a reduced response to pigeon cytochrome c peptide antigen, as determined by ZAP70 phosphorylation, proliferation, and interleukin 2. the production of Tako Stefanova et al. (2002) showed that self-MHC recognition (which, if too strong, can contribute to autoimmune disease) maintains a CD4+ T cell response when foreign antigens are abst.
Pioneering work by Noel Rose and Ernst Vitebsky of New York and Roitt and Doniach of University College London provided clear evidence that antibody-producing B cells (at least for B lymphocytes) are associated with diseases such as rheumatoid arthritis and thyrotoxicosis. loss of immunological tolerance, i.e. the individual’s ability to ignore “self” while reacting to “non-self”. This breakdown causes the immune system to mount an effective and specific immune response against auto-antigens. The exact origin of immune tolerance is still elusive, but in the 20th century. Since the middle of the century, several theories have been proposed to explain its origin.
Tolerance can also be distinguished from “central” and “peripheral” tolerance, depending on whether the control mechanisms described above operate in central lymphoid organs (thymus and bone marrow) or in peripheral lymphoid organs (lymph node, spleen, etc.) . , where self-reactive B-cells can be destroyed). It should be emphasized that these theories are not mutually exclusive, and there is increasing evidence suggesting that all of these mechanisms may actively contribute to immune tolerance in vertebrates.
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A surprising feature of loss of tolerance in spontaneous human autoimmunity is that it is almost exclusively limited to autoantibody responses produced by B lymphocytes. Loss of T cell tolerance has been very difficult to demonstrate, and where there is evidence of an abnormal T cell response, it is usually not to antibodies that recognize autoantibodies. Thus, in rheumatoid arthritis there are autoantibodies against IgG Fc, but to some extent there is no corresponding T cell response. In systemic lupus, there are autoantibodies against DNA that fail to elicit a T-cell response, and limited evidence for T-cell responses implicates nucleoprotein antibodies. In celiac disease, there are autoantibodies against tissue transglutaminase, but the T cell response is on the side of the protein gliadin. This disparity has led to the belief that most human autoimmune diseases (including type I diabetes with a few exceptions) are based on loss of B-cell tolerance, which misuses normal T-cell responses to foreign antibodies.
There are many immunodeficiency syndromes with clinical and laboratory features of autoimmunity. A reduced ability of the immune system to clear infections may be responsible for causing autoimmunity in the constant activation of the immune system.
An example is common variable immunodeficiency (CVID), where multiple autoimmune diseases occur, such as inflammatory bowel disease, autoimmune thrombocytopenia, and autoimmune thyroid disease.
Familial hemophagocytic lymphohistiocytosis, an autosomal recessive primary immunodeficiency, is another example. Pancytopia, rash, swollen lymph nodes, a large part of the liver and spleen are usually present in such individuals. The absence of perforin is thought to be the presence of many unexplained viral infections.
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In addition to chronic and/or recurrent infections, many autoimmune diseases are also seen in arthritis, autoimmune hemolytic anemia, scleroderma, and type 1 diabetes mellitus in X-linked agammaglobulinemia (XLA). Recurrent bacterial and fungal infections and chronic inflammation of the intestines and lungs also occur in chronic granulomatous disease (CGD). CGD is caused by depletion of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase by neutrophils. Hypomorphic RAG mutations occur in patients with central granulomatous disease; an autoimmune disorder that usually occurs in patients with granulomatosis with polyangiitis and NK/T cell lymphomas. Autoimmunity and infections also coexist in autoimmune polydocrinopathy-candidiasis-ectodermal dystrophy: organ-specific autoimmune manifestations (eg, hypoparathyroidism and adrocortical insufficiency) and chronic mucocutaneous candidiasis. Finally, IgA deficiency is sometimes associated with the development of autoimmune and atopic forms.
Certain people are prone to developing autoimmune diseases. This susceptibility is linked to several genes plus other risk factors. Genetically predisposed individuals do not always develop autoimmune diseases. Three main groups of ges are suspected in many autoimmune diseases. The following are related:
The first two, which are involved in antiquities recognition, are inherently variable and capable of recombination. These variants allow the immune system to respond to many invaders, but can also generate lymphocytes capable of self-reactivity.
MHC class I molecules are less closely related. The most significant and complete association is between HLA B27 and spondyloarthropathies such as ankylosing spondylitis and reactive arthritis. Correlations may exist between MHC class II promoter polymorphisms and autoimmune diseases.
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The contributions of genes outside the MHC complex continue to be the subject of research, both in animal models of disease (Linda Wicker’s extensive genetic studies of diabetes in NOD mice) and in mice (Brian Kotzin’s linkage analysis of susceptibility to SLE).
PTPN22 is directly associated with multiple autoimmune diseases, including type I diabetes, rheumatoid arthritis, systemic lupus erythematosus, Hashimoto’s thyroiditis, Graves’ disease, Addison’s disease, myastia gravis, vitiligo, systemic sclerosis, and juvenile idiopathic arthritis.
There is some evidence that a person’s gender may also play a role in the development of autoimmunity; that is, most autoimmune diseases are gender-related. Some autoimmune diseases that are more likely to develop in women include ankylosing spondylitis, type 1 diabetes mellitus, granulomatosis with polyangiitis, Crohn’s disease, primary sclerosing cholangitis, and psoriasis.
The reasons for the role of gender in autoimmunity are varied. Women appear to produce greater inflammatory responses than when their own immune systems are activated, increasing the risk of autoimmunity. The participation of sex steroids in many autoimmune diseases is indicated by hormonal changes, for example: during pregnancy, during the estrous cycle or during the use of oral contraceptives. A history of pregnancy appears to confer an increased risk of autoimmune disease. It is hypothesized that the direct and subtle exchange of cells between mother and child during pregnancy may lead to autoimmunity.
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The false X-inactivation theory proposed by Jeff Stewart of Princeton University has been experimentally confirmed in scleroderma and autoimmune thyroiditis.
There is an interesting inverse relationship between infectious diseases and autoimmune diseases. Autoimmune diseases rarely occur in areas where multiple infectious diseases are endemic. The reverse seems to be true, to some extent. The hygiene hypothesis attributes these correlations to strategies involving immune manipulation of pathogens. Although such an observation is false and ineffective, according to some studies, it is associated with parasite infection.
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