Rheumatoid arthritis (RA) is an autoimmune disorder characterized by chronic inflammation of multiple joints and organs. For many years RA has been recognized as a Th1 mediated disease, but recently Th17 cells appear to play a pivotal role in RA pathogenesis. Studies have revealed that IL-17 producing T cells are important cell types contributing to arthritis. Accordingly, plasticity between different Th1, Th17 and Treg cells has been described, indicating that differentiation of Th subsets is not entirely restricted to separate lineages. Therefore, this report will address these novel insights of pathogenecity and plasticity of different Th subsets in RA
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