Journal
NATURE REVIEWS RHEUMATOLOGY
Volume 10, Issue 3, Pages 160-170Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nrrheum.2013.205
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Funding
- Medical Research Council of Hungary [ETT 315/2009]
- European Union, European Social Fund and Hungary [TAMOP 4.2.1/B-09/1/KONV-2010-0007]
- National Excellence Convergence Program [TAMOP 4.2.1/B-09/1/KONV-2010-0007, TAMOP-4.2.2. A-11/1/KONV-2012-0031]
- NIH [R01 AR059356, R01 AR064206, R21 AR062332]
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The involvement of autoreactive T cells in the pathogenesis of rheumatoid arthritis (RA) as well as in autoimmune animal models of arthritis has been well established; however, unanswered questions, such as the role of joint-homing T cells, remain. Animal models of arthritis are superb experimental tools in demonstrating how T cells trigger joint inflammation, and thus can help to further our knowledge of disease mechanisms and potential therapies. In this Review, we discuss the similarities and differences in T-cell subsets and functions between RA and mouse arthritis models. For example, various T-cell subsets are involved in both human and mouse arthritis, but differences might exist in the cytokine regulation and plasticity of these cells. With regard to joint-homing T cells, an abundance of synovial T cells is present in humans compared with mice. On the other hand, local expansion of type 17 T-helper (TH17) cells is observed in some animal models, but not in RA. Finally, whereas T-cell depletion therapy essentially failed in RA, antibody targeting of T cells can work, at least preventatively, in most arthritis models. Clearly, additional human and animal studies are needed to fill the gap in our understanding of the specific contribution of T-cell subsets to arthritis in mice and men.
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