| First Author | Metwali A | Year | 2021 |
| Journal | Eur J Immunol | Volume | 51 |
| Issue | 2 | Pages | 433-444 |
| PubMed ID | 33067820 | Mgi Jnum | J:302286 |
| Mgi Id | MGI:6506951 | Doi | 10.1002/eji.201848072 |
| Citation | Metwali A, et al. (2021) Helminth-induced regulation of T-cell transfer colitis requires intact and regulated T cell Stat6 signaling in mice. Eur J Immunol 51(2):433-444 |
| abstractText | Infection with parasitic worms (helminths) alters host immune responses and can inhibit pathogenic inflammation. Helminth infection promotes a strong Th2 and T regulatory response while suppressing Th1 and Th17 function. Th2 responses are largely dependent on transcriptional programs directed by Stat6-signaling. We examined the importance of intact T cell Stat6 signaling on helminth-induced suppression of murine colitis that results from T cell transfer into immune-deficient mice. Colonization with the intestinal nematode Heligmosomoides polygyrus bakeri resolves WT T cell transfer colitis. However, if the transferred T cells lack intact Stat6 then helminth exposure failed to attenuate colitis or suppress MLN T cell IFN-gamma or IL17 production. Loss of Stat6 signaling resulted in decreased IL10 and increased IFN-gamma co-expression by IL-17(+) T cells. We also transferred T cells from mice with constitutive T cell expression of activated Stat6 (Stat6VT). These mice developed a severe eosinophilic colitis that also was not attenuated by helminth infection. These results show that T cell expression of intact but regulated Stat6 signaling is required for helminth infection-associated regulation of pathogenic intestinal inflammation. |
