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Pathological role of osteoclast costimulation in arthritis-induced bone loss.

ABSTRACT: Abnormal T cell immune responses induce aberrant expression of inflammatory cytokines such as TNF-alpha, leading to osteoclastmediated bone erosion and osteoporosis in autoimmune arthritis. However, the mechanism underlying enhanced osteoclastogenesis in arthritis is not completely understood. Here we show that TNF-alpha contributes to inflammatory bone loss by enhancing the osteoclastogenic potential of osteoclast precursor cells through inducing paired Ig-like receptor-A (PIR-A), a costimulatory receptor for receptor activator of NF-kappaB (RANK). In fact, bone erosion and osteoporosis, but not inflammation, caused by aberrant TNF-alpha expression were ameliorated in mice deficient in Fc receptor common gamma subunit or beta(2)-microglobulin, in which the expression of PIR-As and PIR-A ligands is impaired, respectively. These results establish the pathological role of costimulatory receptors for RANK in bone loss in arthritis and may provide a molecular basis for the future therapy of inflammatory diseases.

SUBMITTER: Ochi S 

PROVIDER: S-EPMC2040909 | biostudies-other | 2007 Jul

REPOSITORIES: biostudies-other

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Pathological role of osteoclast costimulation in arthritis-induced bone loss.

Ochi Sae S   Shinohara Masahiro M   Sato Kojiro K   Gober Hans-Jürgen HJ   Koga Takako T   Kodama Tatsuhiko T   Takai Toshiyuki T   Miyasaka Nobuyuki N   Takayanagi Hiroshi H  

Proceedings of the National Academy of Sciences of the United States of America 20070625 27

Abnormal T cell immune responses induce aberrant expression of inflammatory cytokines such as TNF-alpha, leading to osteoclastmediated bone erosion and osteoporosis in autoimmune arthritis. However, the mechanism underlying enhanced osteoclastogenesis in arthritis is not completely understood. Here we show that TNF-alpha contributes to inflammatory bone loss by enhancing the osteoclastogenic potential of osteoclast precursor cells through inducing paired Ig-like receptor-A (PIR-A), a costimulato  ...[more]

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