Abstract
Rheumatoid arthritis (RA) was originally thought to be a T-helper (Th)1-, not a Th2-, associated disorder; however, it currently is unclear whether RA is a Th1- and/or Th17-mediated disease, and what the contributions of these T-cell subsets are in the pathogenesis of RA. Results from studies using different arthritis models have demonstrated that IL-17-producing T-cells are the dominant cell type in the development of arthritis. In addition, a critical role of the IL-23/IL-17 axis in the progression to chronic destructive arthritis has been demonstrated. Interestingly, Th1 and Th17 cells both may have unique pathogenic potential, and the recent insights into T-cell plasticity may change the understanding of the role of T-cell subsets in chronic autoimmune diseases.
| Original language | English |
|---|---|
| Pages (from-to) | 452-462 |
| Number of pages | 11 |
| Journal | CURRENT OPINION IN INVESTIGATIONAL DRUGS |
| Volume | 10 |
| Issue number | 5 |
| Publication status | Published - May 2009 |
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