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Several pathological mechanisms have been proposed to explain the development of autoimmune conditions. Aside from the roles played by genetic and environmental factors, some of the main pathological processes proposed are described below:
Normally, B cells are activated by T cells before B cells can produce antibodies in large quantities. However, if the T cells are bypassed and the antigen directly stimulates the B cells, the immune response may be altered.
Healthy immune responses require B and T cell reactions to the same antigen. However, scientists Rosnek and Lanzavecchia showed how B cells that recognize IgGFc can recruit help from any T cell stimulated by an antigen that has been co-endocytosed by a B cell. In celiac disease, for example, it seems B cells that recognize transglutamine are helped by T cells that recognize gliadin.
Altered B cell receptor-mediated feedback may give rise to spontaneous autoimmunity. When an antibody binds to a certain antigen, it may cause aberrent signals to be fed back to B cells through ligands bound to the membrane, such as the B cell receptor, IgGFc receptors, CD21 and toll-like receptors 9 and 7. This forms the basis of the idea that self-perpetuating self reactive B cells can exist.
Structural similarities shared between an exogenous antigen and certain self antigens may result in any antibody produced against the exogenous antigen also binding to the host antigen to flag it up for attack by the immune system. This is thought to be the underlying cause of rheumatic fever, although the exogenous antigen has not yet been formally identified.