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This Sqadia video provide comprehensive details about disease caused by autoimmunity. Survival of clones which are only moderately responsive to self-antigens present in generative organs; forms T cell repertoire. Immunoregulation is a balance between activation and suppression of effector cells to achieve an efficient immune response without damaging the host. B cells binding to autoantigens in the periphery may be excluded from follicles. Excluded B cells undergo apoptosis. Rapid elimination depends on the presence of a normal repertoire of B cells. The induction of tolerance may be exploited to prevent graft rejection, to treat autoimmune and allergic diseases, and to prevent immune responses in gene therapy.
Autoimmunity: Types and Causes
Autoimmunity can be defined as breakdown of mechanisms responsible for self-tolerance and induction of an immune response against components of the self. Both antibodies and effector T cells can be involved in the damage in autoimmune diseases. 1960- it was believed that all self-reactive lymphocytes were eliminated during their development. 1970s- experimental evidence countered that belief revealing that not all self-reactive lymphocytes are deleted. Normal healthy individuals have been shown to possess mature, recirculating, self-reactive lymphocytes- not resulting in autoimmune reactions. Their activity must be regulated in normal individuals through clonal anergy and clonal suppression. A process by which B and T cells are deactivated after they have expressed receptors for self-antigens & before they develop into fully immunocompetent lymphocytes. Anergy is a term in immunobiology that describes a lack of reaction by the body's defense mechanisms to foreign substances. Lymphocytes are said to be anergic when they fail to respond to their specific antigen. The process of switching off the ability of potentially harmful T or B cells to participate in immune responses.
Organ Specific Autoimmune Disease-I
The immune response is directed to a target antigen unique to a single organ or gland, so that the manifestations are largely limited to that organ. Autoimmune diseases involving direct cellular damage occur when lymphocytes or antibodies bind to cell-membrane antigens causing cellular lysis and/or an inflammatory response in the affected organ. Gradually, the damaged cellular structure is replaced by connective tissue (scar tissue), and the function of the organ declines. Auto-antibodies specific for certain basement-membrane antigens bind to the basement membranes of the kidney glomeruli and the alveoli of the lungs. The production of thyroid hormones is carefully regulated by thyroid-stimulating hormone (TSH)- produced by the pituitary gland. A patient with Graves’ disease produces auto-antibodies that bind the receptor for TSH. Myasthenia gravis is the prototype autoimmune disease mediated by blocking antibodies.
Organ Specific Autoimmune Disease-II
Addison's disease is a disorder that occurs when your body produces insufficient amounts of certain hormones produced by adrenal glands. In Addison's disease, your adrenal glands produce too little cortisol and often insufficient levels of aldosterone as well. Antibodies detected against FSH could be natural antibodies also subjected to pregnancy-associated immune system regulations. Anti-FSH IgA detected in female circulation could be a part of the mucosal response involved in inducing immune tolerance to seminal constituents. Anti-FSH IgM associates with the peripheral level of FSH hormone and possibly contributes along with the mucosal-associated induction of IgA to the production of circulating anti-FSH IgG.
Systemic Autoimmune Disease
The response is directed toward a broad range of target antigens and involves a number of organs and tissues hyperactive T cells and B cells are involved. In women between 20 and 40 years of age; the ratio of female to male patients is 10:1. SLE is characterized by fever, weakness, arthritis, skin rashes, pleurisy, and kidney dysfunction. Lupus is more frequent in African-American and Hispanic women than in Caucasians. Affected individuals may produce autoantibodies to a vast array of tissue antigens, such as DNA, histones, RBCs, platelets, leukocytes, and clotting factors. Interaction of these auto-antibodies with their specific antigens produces various symptoms. Auto-antibody specific for RBCs and platelets, for example, can lead to complement-mediated lysis, resulting in hemolytic anemia and thrombocytopenia. When immune complexes of auto-antibodies with various nuclear antigens are deposited along the walls of small blood vessels, a type III hypersensitive reaction develops.