IL-23 induces receptor activator of NF-kappaB ligand expression on CD4+ T cells and promotes osteoclastogenesis in an autoimmune arthritis model |
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Authors: | Ju Ji Hyeon Cho Mi-La Moon Young-Mee Oh Hye-Joa Park Jin-Sil Jhun Joo-Youn Min So-Youn Cho Young-Gyu Park Kyung-Su Yoon Chong-Hyeon Min Jun-Ki Park Sung-Hwan Sung Young-Chul Kim Ho-Youn |
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Institution: | The Center for Rheumatic Diseases, Kangnam St Mary's Hospital, and Rheumatism Research Center, College of Medicine, The Catholic University of Korea, Seoul, South Korea. |
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Abstract: | IL-23, a clinically novel cytokine, targets CD4(+) T cells. Recent IL-1Ra(-/-) mouse studies have demonstrated that IL-23 indirectly stimulates the differentiation of osteoclast precursors by enhancing IL-17 release from CD4(+) T cells. IL-17, in turn, stimulates osteoclastogenesis in osteoclast precursor cells. In this study, we found that IL-23 up-regulates receptor activator of NF-kappaB ligand expression by CD4(+) T cells, and thus contributes to osteoclastogenesis. This indirect pathway is mediated by NF-kappaB and STAT3. We have also demonstrated that IL-23 can influence osteoclastogenesis positively under the special conditions in the IL-1-dominant milieu of IL-1Ra(-/-) mice. We propose that IL-23-enhanced osteoclastogenesis is mediated mainly by CD4(+) T cells. The results of this study show that IL-23 is a promising therapeutic target for the treatment of arthritis-associated bone destruction. |
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