Abstract
IL-17 secreting helper CD4 T cells (Th17 cells) contribute to a variety of autoimmune diseases such as rheumatoid arthritis. IL-17 acts on neutrophils, macrophages, fibroblasts, or osteocalsts to mediate chronic inflammation and destroy the cartilage. Recently, studies of the spontaneous models of arthritis revealed that activation of innate immunity, such as Toll like receptors, C-type lectin receptors, complement, or ATP induce IL-6 or IL-23 production from macrophages or dendritic cells, which triggers the differentiation of Th17 cells and induces autoimmune arthritis. Although the role of Th17 cells in human rheumatoid arthritis is still controversial, activation of innate immunity and induction of Th17 cells should be associated with the induction of arthritis at least in a part of RA patients. These studies will help elucidate the mechanism of arthritis induction and discover the therapeutic method to prevent it.
