| First Author | Rani R | Year | 2011 |
| Journal | Eur J Immunol | Volume | 41 |
| Issue | 7 | Pages | 2000-9 |
| PubMed ID | 21469118 | Mgi Jnum | J:177315 |
| Mgi Id | MGI:5294729 | Doi | 10.1002/eji.201041135 |
| Citation | Rani R, et al. (2011) TGF-beta limits IL-33 production and promotes the resolution of colitis through regulation of macrophage function. Eur J Immunol 41(7):2000-9 |
| abstractText | Mvarphis promote tissue injury or repair depending on their activation status and the local cytokine milieu. It remains unclear whether the immunosuppressive effects of transforming growth factor beta (TGF-beta) serve a nonredundant role in Mvarphi function in vivo. We generated Mvarphi-specific transgenic mice that express a truncated TGF-beta receptor II under control of the CD68 promoter (CD68TGF-betaDNRII) and subjected these mice to the dextran sodium sulfate (DSS) model of colitis. CD68TGF-betaDNRII mice have an impaired ability to resolve colitic inflammation as demonstrated by increased lethality, granulocytic inflammation, and delayed goblet cell regeneration compared with transgene negative littermates. CD68TGF-betaDNRII mice produce significantly less IL-10, but have increased levels of IgE and numbers of IL-33+ Mvarphis than controls. These data are consistent with associations between ulcerative colitis and increased IL-33 production in humans and suggest that TGF-beta may promote the suppression of intestinal inflammation, at least in part, through direct effects on Mvarphi function. |
