| First Author | Ribot JC | Year | 2010 |
| Journal | J Immunol | Volume | 185 |
| Issue | 11 | Pages | 6421-6425 |
| PubMed ID | 21037088 | Mgi Jnum | J:166145 |
| Mgi Id | MGI:4839835 | Doi | 10.4049/jimmunol.1002283 |
| Citation | Ribot JC, et al. (2010) Cutting Edge: Adaptive Versus Innate Receptor Signals Selectively Control the Pool Sizes of Murine IFN-{gamma}- or IL-17-Producing {gamma}{delta} T Cells upon Infection. J Immunol 185(11):6421-5 |
| abstractText | gammadelta T lymphocytes are commonly viewed as embracing properties of both adaptive and innate immunity. Contributing to this is their responsiveness to pathogen products, either with or without the involvement of the TCR and its coreceptors. This study clarifies this paradoxical behavior by showing that these two modes of responsiveness are the properties of two discrete sets of murine lymphoid gammadelta T cells. Thus, MyD88 deficiency severely impaired the response to malaria infection of CD27((-)), IL-17A-producing gammadelta T cells, but not of IFN-gamma-producing gammadelta cells. Instead, the latter compartment was severely contracted by ablating CD27, which synergizes with TCRgammadelta in the induction of antiapoptotic mediators and cell cycle-promoting genes in CD27((+)), IFN-gamma-secreting gammadelta T cells. Hence, innate versus adaptive receptors differentially control the peripheral pool sizes of discrete proinflammatory gammadelta T cell subsets during immune responses to infection. |
