| First Author | Kishida K | Year | 2015 |
| Journal | Int Immunol | Volume | 27 |
| Issue | 6 | Pages | 307-14 |
| PubMed ID | 25710489 | Mgi Jnum | J:230913 |
| Mgi Id | MGI:5766444 | Doi | 10.1093/intimm/dxv004 |
| Citation | Kishida K, et al. (2015) Negative regulation of DSS-induced experimental colitis by PILRalpha. Int Immunol 27(6):307-14 |
| abstractText | Inflammatory bowel disease is thought to be a complex multifactorial disease, in which an increased inflammatory response plays an important role. Paired immunoglobulin-like type 2 receptor alpha (PILRalpha), well conserved in almost all mammals, is an inhibitory receptor containing immunoreceptor tyrosine-based inhibitory motifs in the cytoplasmic domain. PILRalpha is mainly expressed on myeloid cells and plays an important role in the regulation of inflammation. In the present study, we investigated the function of PILRalpha in inflammatory bowel disease using PILRalpha-deficient mice. When mice were orally administered dextran sulfate sodium (DSS), colonic mucosal injury and inflammation were significantly exacerbated in DSS-treated PILRalpha-deficient mice compared with wild-type (WT) mice. Flow cytometric analysis revealed that neutrophil and macrophage cell numbers were higher in the colons of DSS-treated PILRalpha-deficient mice than in those of WT mice. Blockade of CXCR2 expressed on neutrophils using a CXCR2 inhibitor decreased the severity of colitis observed in PILRalpha-deficient mice. These results suggest that PILRalpha negatively regulates inflammatory colitis by regulating the infiltration of inflammatory cells such as neutrophils and macrophages. |
