Author(s): Toh ML, Miossec P
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PURPOSE OF REVIEW:
To update the knowledge on the contribution of T cells in rheumatoid arthritis, a selection of publications between the end of 2005 and 2006 were reviewed.
Th17 cells driven by TGF-beta, IL-1, IL-6 and IL-23 challenge previous concepts of 'Th1'-induced rheumatoid arthritis. Other advancements in IL-17 studies include novel concepts on the IL-17 receptor and additional information on the mechanism of IL-17-induced effects. Regulatory T cells fail to control disease due to defective function secondary to the synovial inflammatory milieu. The predominance of pathogenic effector T cells in the presence of impaired T-cell regulatory mechanisms may therefore contribute to rheumatoid arthritis chronicity. Cellular therapies attempt to restore the balance that includes production of immunoregulatory cytokines such as IL-4 or IL-10. Better T-cell-targeted therapies controlling costimulation are in place with purported increased efficacy and durability, including anti-tumour necrosis factor nonresponders. Additional direct and indirect T-cell approaches include antagonism of T-cell-derived cytokines, T-cell activation or B-cell ablation.
A renewed interest in T cells comes from the discovery of Th17 in rheumatoid arthritis and from novel findings on the role of T cells in rheumatoid arthritis induction, chronicity and relapse.
This article was published in CurrOpinRheumatol
and referenced in Immunotherapy: Open Access