| First Author | Buus TB | Year | 2016 |
| Journal | Oncotarget | Volume | 7 |
| Issue | 15 | Pages | 19341-54 |
| PubMed ID | 27235509 | Mgi Jnum | J:321320 |
| Mgi Id | MGI:6819327 | Doi | 10.18632/oncotarget.8464 |
| Citation | Buus TB, et al. (2016) Development of interleukin-17-producing Vgamma2+ gammadelta T cells is reduced by ICOS signaling in the thymus. Oncotarget 7(15):19341-54 |
| abstractText | Co-stimulation is an integral part of T cell signaling involved in almost all facets of T cell biology. While much is known about co-stimulation in differentiation and function of conventional alphabeta T cells, less is known about how co-stimulation affects the development and programming of gammadelta T cells. In this study, we have investigated the role of inducible T cell co-stimulator (ICOS) on the development of gammadelta T cells. We show that ICOS is expressed by a population of immature Vgamma2+CD45RBlow gammadelta T cells predisposed to interleukin-17 (IL-17) production. We found that treatment with ICOS specific antibodies drastically reduces fetal development of IL-17-producing gammadelta T cells by agonistic actions, and that ICOS deficient mice have a significant increase in the population of IL-17-producing Vgamma2+ gammadelta T cells in the thymus, spleen, lymph nodes and skin and exhibit exacerbated sensitization responses to 2,4-dinitrofluorobenzene. In conclusion, this study demonstrates that development of IL-17-producing Vgamma2+ gammadelta T cells is reduced by ICOS signaling in the thymus. |
