Presented here is a discussion on how components delineated in the theory of autoantigen complementarity potentially promote the acquisition of multiple 'hallmarks' of disease.
eBook Title: Autoantigen Complementarity and Its Contributions to Hallmarks of Autoimmune Disease
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Published on 2015 by
Abstract: The question considered is, |What causes the autoimmune response to begin and what causes it to worsen into autoimmune disease?| The theory of autoantigen complementarity posits that the initiating immunogen causing disease is a protein complementary (antisense) to the self-antigen, rather than a response to the native protein. The resulting primary antibody elicits an anti-antibody response or anti-idiotype, consequently producing a disease-inciting autoantibody. Yet, not everyone who developes self-reactive autoantibodies will manifest autoimmune disease. What is apparent is that manifestation of disease is governed by the acquisition of multiple immune-compromising traits that increase susceptibility and drive disease. Taking into account current cellular, molecular, and genetic information, six traits, or 'hallmarks', of autoimmune disease were proposed: (1) Autoreactive cells evade deletion, (2) Presence of asymptomatic autoantibodies, (3) Hyperactivity of Fc–FcR pathway, (4) Susceptibility to environmental impact, (5) Antigenic modifications of self-proteins, (6) Microbial Infections. Presented here is a discussion on how components delineated in the theory of autoantigen complementarity potentially promote the acquisition of multiple 'hallmarks' of disease. Highlights: Autoimmune disease is driven by acquisition of multiple immune-compromising traits. Autoantigen complementarity mechanistically promotes disease-associated traits. Six key hallmarks are linked with autoantibody-mediated autoimmune disease.
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