| First Author | Maruhashi T | Year | 2015 |
| Journal | J Immunol | Volume | 194 |
| Issue | 12 | Pages | 5681-91 |
| PubMed ID | 25926676 | Mgi Jnum | J:329133 |
| Mgi Id | MGI:6756589 | Doi | 10.4049/jimmunol.1500273 |
| Citation | Maruhashi T, et al. (2015) DCIR maintains bone homeostasis by regulating IFN-gamma production in T cells. J Immunol 194(12):5681-91 |
| abstractText | 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. |
