Study opens pathway to better diagnosis and treatment of autoimmune diseases. Researchers from Washington University, Stanford University, and Oxford University have developed a method to identify protein fragments and immune cells that cause autoimmune reactions. The study focuses on the HLA-B*2
has developed a way to find crucial protein fragments that drive autoimmunity, as well as the immune cells that respond to them. The findings, published in the journal“Of all genes, the HLA genes have the greatest amount of variation across the human population. There are many, many autoimmune diseases that are associated with specific variants of the HLA genes, and in most cases, we don’t know why,” said co-senior author Wayne M. Yokoyama, MD, the Sam J.
T cells don’t recognize protein fragments by themselves; they recognize the fragment plus the hand that holds it. Scientists have long assumed that the combination of this particular hand — HLA-B*27 — plus a bit of an unknown human protein was being misidentified as dangerous in people with either of the two diseases, triggering autoimmune attacks in the eye or the spine. But for decades, they couldn’t find the fragment.
“This study reveals the power of studying T cell specificity and activity from the ground up; that is, identifying the T cells that are most active in a given response, followed by identifying what they respond to,” Garcia said. “Clearly these patient-derived TCRs are seeing a spectrum of common antigens, and that may be driving the autoimmunity. Proving this in humans is very difficult, but that is our future direction and could lead to therapeutics.
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