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A possible mechanism of osteoclast formation by activated T cells in rheumatoid arthritis
figure
posted on 2011-12-30, 22:12 authored by Nobuyuki Udagawa, Shigeru Kotake, Naoyuki Kamatani, Naoyuki Takahashi, Tatsuo SudaCopyright information:
Taken from "The molecular mechanism of osteoclastogenesis in rheumatoid arthritis"
Arthritis Research 2002;4(5):281-289.
Published online 12 Apr 2002
PMCID:PMC128939.
Copyright © 2002 BioMed Central Ltd
Activated T cells present in the synovial tissues also produce membrane-associated RANKL, some of which are cleaved enzymatically from the plasma membrane, resulting in soluble RANKL (sRANKL). Activated T cells also produce IL-17, which induces RANKL via prostaglandin E synthesis in osteoblasts. IL-6 together with soluble IL-6 receptors (sIL-6R), IL-1-α and TNF-α derived from macrophages induce RANKL in osteoblasts. In addition, TNF-α directly acts on osteoclast progenitors, which then differentiate into osteoclasts by a mechanism independent of the RANKL–RANK interaction. IL-1 also induces osteoclast activation directly. OPG, osteoprotegerin.