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Mechanism of arthritic bone destruction: the critical role of RANKL on synovial fibroblasts and T cells. Activated T cells stimulate the macrophages to secrete proinflammatory cytokines such as TNF-a and IL-1, which strongly induce RANKL on synovial fibroblasts. In addition, T cells themselves also express RANKL. In constrast, there is a very low level of IFN-g, a potent RANKL inhibitor produced by T cells. This imbalance may be responsible for the aberrant activation of osteoclast formation in arthritis. |