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• W1981931003 endingPage "532" @default.
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• W1981931003 abstract "Autoreactive B cells are present in the normal individual. These cells are not normally induced to release their destructive autoantibodies; T cells regulate the responsiveness of the B-cell population, and self-reactive T cells are normally absent. Modification of an epitope on a self component, or immunization with antigens that are cross reactive with self components, can lead to autoantibody formation. This phenomenon has been explained by linked recognition of self epitopes by the autoreactive B cell and the foreign epitopes by inducive T cells. The new concept of antigen processing requires degradation of epitopes on an antigen molecule and their representation as peptides associated with the major histocompatibility complex (MHC) antigens of the antigen presenting cell (APC); the autoreactive B cell can be the APC. A revised model for autoreactive B-cell activation is presented in this paper. This model shows how linkage of foreign and self epitopes can lead to autoantibody formation in a system where antigen is degraded and presented in a peptide form by the APC. Cyclosporine acts by blocking the function of primed T cells. In this way, the drug prevents induction of autoreactive B cells. Specifically, cyclosporine acts by blocking the production of messenger RNA for lymphokine production. The agent does not block T-cell priming in vivo. Thus, while cyclosporine can provide effective control of autoimmunity, drug levels must be maintained to prevent disease relapse." @default.
• W1981931003 created "2016-06-24" @default.
• W1981931003 creator A5029188597 @default.
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• W1981931003 date "1988-12-01" @default.
• W1981931003 modified "2023-09-23" @default.
• W1981931003 title "Cyclosporine A and the regulation of autoimmune disease" @default.
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• W1981931003 doi "https://doi.org/10.1016/0896-8411(88)90045-5" @default.
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