DCIR maintains bone homeostasis by regulating IFN-γ production in T cells

Takumi Maruhashi, Tomonori Kaifu, Rikio Yabe, Akimasa Seno, Soo Hyun Chung, Noriyuki Fujikado, Yoichiro Iwakura

研究成果: Article査読

15 被引用数 (Scopus)

抄録

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-γ 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-γ-producing T cells accumulated in lymph nodes and joints of Dcir-/- mice, and purified Dcir-/- DCs enhanced IFN-γ+ T cell differentiation. The ankylotic changes and bone volume increase were suppressed in the absence of IFN-γ. Thus, IFN-γ 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.

本文言語English
ページ(範囲)5681-5691
ページ数11
ジャーナルJournal of Immunology
194
12
DOI
出版ステータスPublished - 15 6 2015

フィンガープリント

「DCIR maintains bone homeostasis by regulating IFN-γ production in T cells」の研究トピックを掘り下げます。これらがまとまってユニークなフィンガープリントを構成します。

引用スタイル