期刊
JOURNAL OF IMMUNOLOGY
卷 194, 期 12, 页码 5681-5691出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1500273
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资金
- Japan Society for the Promotion of Science [24220011, 23500489]
- Japan Science and Technology Agency
- Science and Technology Research Promotion Program for Agriculture, Forestry, Fisheries, and Food Industry
- Grants-in-Aid for Scientific Research [23500489, 26430095] Funding Source: KAKEN
Dendritic cell immunoreceptor (DCIR) is a C-type lectin receptor mainly expressed in DCs. Dcir(-/-) mice spontaneously develop autoimmune enthesitis and ankylosis accompanied by fibrocartilage proliferation and ectopic ossification. However, the mechanisms of new bone/cartilage formation in Dcir(-/-) mice remain to be elucidated. In this study, we show that DCIR maintains bone homeostasis by regulating IFN-gamma production under pathophysiological conditions. DCIR deficiency increased bone volume in femurs and caused aberrant ossification in joints, whereas these symptoms were abolished in Rag2(-/-) Dcir(-/-) mice. IFN-gamma producing T cells accumulated in lymph nodes and joints of Dcir(-/-) mice, and purified Dcir(-/-) DCs enhanced IFN-gamma(+) T cell differentiation. The ankylotic changes and bone volume increase were suppressed in the absence of IFN-gamma. Thus, IFN-gamma is a positive chondrogenic and osteoblastogenic factor, and DCIR is a crucial regulator of bone metabolism; consequently, both factors are potential targets for therapies directed against bone metabolic diseases.
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