Evidence of autoimmunity's origins uncovered via new approach WUSTLmedschool nature
That finally may be changing. A team involving researchers from Washington University School of Medicine in St. Louis, Stanford University School of Medicine and Oxford University 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 Dec. 7 in"Of all genes, the HLA genes have the greatest amount of variation across the. 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. Levin and Audrey Loew Levin Professor of Arthritis Research at Washington University."This paper outlines a strategy for figuring out why certain HLA variants are linked to certain diseases. It also provides strong evidence that cross-reactivity between human and microbial proteins drives autoimmunity in at least two diseases and probably many others. Now that we understand the underlying drivers, we can start focusing on the approaches that are most likely to yield benefits for patients." The autoimmune diseases ankylosing spondylitis, which involves arthritis in the spine and pelvis, and acute anterior uveitis, which is characterized by inflammation in the eye, are both strongly associated with an HLA variant called HLA-B*27. The link between ankylosing spondylitis and HLA-B*27 was discovered 50 years ago—making it one of the first such associations identified betweenand HLA variants—and it remains one of the strongest known associations between any disease and an HLA variant. The HLA family of proteins is involved in helping immune cells detect invading pathogens and distinguishing between microbial and human proteins, and is highly variable across individuals. HLA proteins function like hands that pick up fragments of whichever proteins are lying about—microbial or human—and show them toT 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. Some scientists began to speculate that the misidentification hypothesis was wrong and some other reason accounted for the association between HLA-B*27 and the two diseases. Co-corresponding author K. Christopher Garcia, Ph.D., and co-first author Xinbo Yang, Ph.D., of Stanford Medicine, along with co-corresponding authors Geraldine M. Gillespie, Ph.D., and Andrew J. McMichael, Ph.D., and co-first author Lee Garner, Ph.D., of Oxford University, collaborated with Yokoyama and co-first author Michael Paley, MD, Ph.D., of Washington University on a novel way to find the elusive fragment. The research team identified certain T cells that were abundant in the blood and joints of people with ankylosing spondylitis, and in the eyes of people with uveitis.
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