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- W1997585969 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." @default.
- W1997585969 created "2016-06-24" @default.
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- W1997585969 date "2007-07-03" @default.
- W1997585969 modified "2023-10-14" @default.
- W1997585969 title "Pathological role of osteoclast costimulation in arthritis-induced bone loss" @default.
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- W1997585969 doi "https://doi.org/10.1073/pnas.0701971104" @default.
- W1997585969 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2040909" @default.
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