Broad Institute of MIT and Harvard’s Post

For 50 years, scientists have pondered why variants in the gene HLA-B27 increase a person's risk of developing spondyloarthritis and similar rheumatic conditions by up to 200-fold. In a Cell Chemical Biology review, Eric Brown, Phuong Nguyen, and Ramnik Xavier discuss recent advances in the search for how environmental triggers such as the microbiome could interact with HLA-B27 to initiate rheumatic disease. Variants in the gene change the shape of its protein's peptide binding groove and may set off an autoimmune response involving CD8+ T cells, which can trigger inflammation depending on the metabolic context. The authors suggest future research using computational modeling to predict peptide interactions. #BroadInstitute #Science #ScienceNews #Research #ScientificResearch #Microbiome #Arthritis

Emerging biochemical, microbial and immunological evidence in the search for why HLA-B∗27 confers risk for spondyloarthritis

Emerging biochemical, microbial and immunological evidence in the search for why HLA-B∗27 confers risk for spondyloarthritis

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