| First Author | Do JS | Year | 2017 |
| Journal | J Immunol | Volume | 198 |
| Issue | 2 | Pages | 908-915 |
| PubMed ID | 27927968 | Mgi Jnum | J:252184 |
| Mgi Id | MGI:5925902 | Doi | 10.4049/jimmunol.1601060 |
| Citation | Do JS, et al. (2017) gammadelta T Cells Coexpressing Gut Homing alpha4beta7 and alphaE Integrins Define a Novel Subset Promoting Intestinal Inflammation. J Immunol 198(2):908-915 |
| abstractText | gammadelta T lymphocytes, dominant T cell subsets in the intestine, mediate both regulatory and pathogenic roles, yet the mechanisms underlying such opposing effects remain unclear. In this study, we identified a unique gammadelta T cell subset that coexpresses high levels of gut-homing integrins, CD103 and alpha4beta7. They were exclusively found in the mesenteric lymph node after T cell-mediated colitis induction, and their appearance preceded the inflammation. Adoptive transfer of the CD103+alpha4beta7high subsets enhanced Th1/Th17 T cell generation and accumulation in the intestine, and the disease severity. The level of generation correlated with the disease severity. Moreover, these cells were also found to be elevated in a spontaneous mouse model of ileitis. Based on the procolitogenic function, we referred to this subset as "inflammatory" gammadelta T cells. Targeting inflammatory gammadelta T cells may open a novel strategy to treat inflammatory diseases where gammadelta T cells play a pathogenic role including inflammatory bowel disease. |
