AI Article Synopsis
- Autoimmunity remains a complex and poorly understood area within clinical immunology, with unclear causes involving genetic, environmental, and immune system factors.
- Molecular mimicry, where the immune system mistakenly targets the body's own cells after responding to infectious agents, is a key concept in understanding autoimmune disorders.
- Current research focuses on identifying specific infectious agents and their links to autoimmunity, which could lead to new prevention and treatment strategies for these conditions.
Article Abstract
Autoimmunity is still a mystery of clinical immunology and medicine as a whole. The etiology and pathogenesis of autoimmune disorders remain unclear and, thus, are assessed as a balance between hereditary predisposition, triggering factors and the appearance of autoantibodies and/or self-reactive T cells. Among the immunological armamentarium, molecular mimicry, based on self-reactive T- and B-cell activation by cross-reactive epitopes of infectious agents, is of special value. Hypotheses regarding the possible involvement of molecular mimicry in the development of postinfectious autoimmunity are currently very intriguing. They provide new approaches for identifying etiological agents that are associated with postinfectious autoimmunity, paired microbial- and tissue-linked epitopes targeted for autoimmune reaction determination, postinfectious autoimmunity pathogenesis recognition and specific prevention, and therapy for autoimmune disorder development.
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