Researchers from Washington University, Stanford, and Oxford University have unveiled a method to identify the protein fragments and immune cells implicated in autoimmune reactions, with a particular focus on the HLA-B*27 variant associated with ankylosing spondylitis and acute anterior uveitis. The study suggests that T cells misidentify normal human proteins as threats due to their similarity to bacterial proteins, leading to autoimmune diseases. Despite decades of research, pinpointing the exact human protein fragment that triggers this confusion had remained elusive.
The team developed a novel approach to identify T cells prevalent in patients with these conditions and mapped the protein fragments recognized by these T cells. They found that T cell receptors (TCRs) responding to HLA-B*27 displayed substantial similarities between responses to microbial and human proteins. This discovery supports the theory that cross-reactivity between human and microbial proteins may drive autoimmune responses.
These findings could significantly enhance diagnostics and treatments for autoimmune diseases by accelerating the identification of disease-causing T cells and enabling earlier intervention. The research indicates promising implications for developing targeted therapies, potentially offering new avenues for curing or preventing these conditions in genetically predisposed individuals.
