Negative selection, epitope mimicry and autoimmunity. (December 2017)

• Record Type: Journal Article
• Authors: Rose, Noel R
• Is Part Of: Current opinion in immunology. Volume 49(2017)
• Page Start: 51
• Page End: 55
• Publication Date: 2017-12
• Subjects: Immunology -- Periodicals; Allergy -- Periodicals; Immunology -- Abstracts -- Periodicals; Allergy -- Abstracts -- Periodicals; 616.079
• DOI: 10.1016/j.coi.2017.08.014
• Languages: English
• ISSNs: 0952-7915

Abstract

Highlights: Cross-reactions between epitopes of an invading microorganism and similar epitopes in the host are common. Only rarely is epitope mimicry known to cause an autoimmune disease in humans. These cross-reactions based on shared epitopes reflects the requirement to maintain a maximal immunologic repertoire. Identifying epitope mimicry opens opportunities for improved treatments and prevention of autoimmune disease. Abstract : Infections often precede the onset of autoimmune disease and molecular (or epitope) mimicry is a plausible link. Cross-reacting epitopes are common between an infecting microorganism and the host because negative selection of self-reactive T-cells and B-cells is frequently incomplete. Complete eradication could lead to major voids in the immunologic repertoire. The association of an autoimmune disease with a microbial epitope may signify a causal relationship with the organism, an indirect connection through bystander effects, persistent infection or coincidence. There are well-established examples of a microbial mimic inducing a defined model of autoimmune disease in experimental animals but such instances are still relatively rare in humans. Establishing epitope mimicry as a direct cause opens opportunities for preventing the disease. Current approaches to cancer immunotherapy provides new examples of epitope mimicry between cancer antigens and normal tissue antigens.