Evidence of autoimmunity’s origins uncovered via new approach

Study opens pathway to better diagnosis, treatment of autoimmune diseases

A T cell receptor that recognizes a human protein fragment (left) is remarkably similar to one that recognizes a bacterial protein fragment (right), and to two receptors capable of recognizing both human and bacterial protein fragments (middle). A study by researchers at Washington University School of Medicine in St. Louis and colleagues at Stanford University and Oxford University supports the idea that some T cells that react to microbes also may react to normal human proteins, causing autoimmune disease. The findings promise to accelerate efforts to improve diagnostic tools and treatments for autoimmune diseases.

In a recent issue of Nature, Drs. Michael Paley and Wayne Yokoyama collaborated with investigators at Stanford and Oxford to identify the potential antigens that may drive anky-
losing spondylitis and acute anterior uveitis. This work suggests that the pathogenesis of HLA-B27-associated disease may be driven by molecular mimicry, where the immune system initially responds to bacterial antigens and then subsequently recognizes similar self-antigens as foreign, leading to disease.