Autoimmunity, epitope analysis, and molecular mimicry

Infectious agents are potential triggers for autoimmune diseases (ADs) in susceptible individuals, with infection being a key factor in initiating autoimmunity. Epidemiological and experimental evidence suggests molecular mimicry as a plausible mechanism for breaking peripheral tolerance, leading to clinical disease. However, molecular mimicry is not the sole mechanism; other factors, such as deficiencies in central tolerance, bystander activation, epitope spreading, and sustained antigenic stimulation, may also contribute to AD etiology. Advanced methods, including molecular docking simulations, affinity estimation for human leukocyte antigens, and three-dimensional structural analysis of peptides, are increasingly vital for studying molecular mimicry’s role in AD pathogenesis. Further research into peptide conformational analysis is essential for designing effective vaccines and understanding environmental factors in autoimmunity.