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The role of T cells in rheumatoid arthritis

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Weyand C. M., Bryl E., Goronzy J. J.

Archivum Immunologiae et Therapiae Experimentalis

2000

vol. 48

issue 5

429-435

In rheumatoid arthritis (RA), T cells infiltrate into the synovial membrane where they initiate and maintain activation of macrophages and synovial fibroblasts, transforming them into tissue-destructive effector cells. The diversity of the disease process and the formation of complex lymphoid microstructures indicates that multiple T cell activation pathways are involved. This model is supported by the association of distinct disease patterns with different variants and combinations of HLA class II molecules. T cell pathology in RA, however, is not limited to the joint. Affected patients have major abnormalities in the T cell pool with a marked contraction in T cell receptor diversity and an outgrowth of large clonal populations. Clonally expanded CD4+ T cells lose expression of the CD28 molecule and gain expression of perforin and granzyme. Consequently, the functional profile of expanded CD4+CD28null T cells is fundamentally changed and is shifted towards tissue-injurious capabilities. CD4+CD28null T cells are particularly important in patients with extraarticular manifestations of RA, where they may have a direct role in vascular injury. Understanding the mechanisms underlying the loss of T cell diversity and the emergence of pro-inflammatory CD4+CD28- T cell clonotypes may have implications for other autoimmune syndromes.

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1 Archivum Immunologiae et Therapiae Experimentalis

1 2000

1 Bryl E.

1 Goronzy J. J.

1 Weyand C. M.

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The role of T cells in rheumatoid arthritis