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- Title
Signal-transducing adaptor protein-2 regulates macrophage migration into inflammatory sites during dextran sodium sulfate induced colitis.
- Authors
Fujita, Natsuko; Oritani, Kenji; Ichii, Michiko; Yokota, Takafumi; Saitoh, Norimitsu; Okuzaki, Daisuke; Sekine, Yuichi; Kon, Shigeyuki; Muromoto, Ryuta; Saitoh, Kodai; Yoshimura, Akihiko; Matsuda, Tadashi; Kanakura, Yuzuru
- Abstract
Signal-transducing adaptor protein-2 (STAP-2) was cloned as a c-fms/M-CSF receptor interacting protein. STAP-2 is an adaptor protein carrying pleckstrin homology and Src homology 2 like domains, as well as a YXXQ motif. STAP-2 has been indicated to have an ability to bind and modulate a variety of signaling and transcriptional molecules. Especially, our previous in vitro studies showed that STAP-2 is crucial for immune and/or inflammatory responses. Here, we have investigated the role of STAP-2 in intestinal inflammation in vivo. The disruption of STAP-2 attenuates dextran sodium sulfate induced colitis via inhibition of macrophage recruitment. To study whether hematopoietic or epithelial cell derived STAP-2 is required for this phenomenon, we generated BM chimeric mice. STAP-2-deficient macrophages impair the ability of CXCL12-induced migration. Intriguingly, STAP-2 also regulates production of proinflammatory chemokines and cytokines such as CXCL1 and TNF-α from intestinal epithelial cells. Therefore, STAP-2 has a potential to regulate plural molecular events during pathological inflammatory responses. Furthermore, our findings not only indicate that STAP-2 is important in regulating intestinal inflammation, but also provide new insights toward the development of novel therapeutic approaches.
- Publication
European Journal of Immunology, 2014, Vol 44, Issue 6, p1791
- ISSN
0014-2980
- Publication type
Article
- DOI
10.1002/eji.201344239