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T-cell and T-cell receptor abnormalities in the immunopathogenesis of juvenile rheumatoid arthritis.

作者信息

Grom A A, Hirsch R

机构信息

William S. Rowe Division of Rheumatology, Children's Hospital Medical Center, Cincinnati, Ohio 45229, USA.

出版信息

Curr Opin Rheumatol. 2000 Sep;12(5):420-4. doi: 10.1097/00002281-200009000-00012.

Abstract

Several lines of indirect evidence suggest that the pathologic autoimmune responses in juvenile rheumatoid arthritis may be antigen-driven and T cell-mediated. These include (1) activation markers expressed on synovial T cells suggestive of previous activation in vivo; (2) persistent oligoclonally expanded T-cell populations accumulating preferentially in the synovial compartment; (3) some T-cell receptor complementarity-determining region 3 sequence similarities between different clones in an individual patient; and (4) T-cell derived cytokines of predominantly Th1 type. Whether T-cell contribution is limited to only early stages of the disease (as appears to be the case in collagen-induced arthritis) or T cells are required for the perpetuation of the inflammation at later stages as well, still remains to be determined.

摘要

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