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Whether autoimmune mechanisms play a role in the pathogenesis of inclusion bo dy myositis (IBM) is unknown. Human leukocyte antigen (HLA) analysis in 52 patie nts, including 17 with autoimmune disorders (AIDs), showed that patients were mo re likely to have antigens from the autoimmune-prone HLA-B8-DR3 ancestral haplotype than healthy control subjects, irrespective of the presence of AIDs. P atients lacked the apparently protective HLA-DR53 antigen. The results provide further support for an autoimmune basis in IBM.
Whether autoimmune mechanisms play a role in the pathogenesis of inclusion bo dy myositis (IBM) is unknown. Human leukocyte antigen (HLA) analysis in 52 patients, including 17 with autoimmune disorders (AIDs), showed that patients were mo re likely to have Antigens from the autoimmune-prone HLA-B8-DR3 ancestral haplotype than healthy control subjects, irrespective of the presence of AIDs. P atients lacked the apparently protective HLA-DR53 antigen. The results provide further support for an autoimmune basis in IBM.