| First Author | Inoue SI | Year | 2017 |
| Journal | Eur J Immunol | Volume | 47 |
| Issue | 4 | Pages | 685-691 |
| PubMed ID | 28012161 | Mgi Jnum | J:291643 |
| Mgi Id | MGI:5924337 | Doi | 10.1002/eji.201646699 |
| Citation | Inoue SI, et al. (2017) Preferentially expanding Vgamma1+ gammadelta T cells are associated with protective immunity against Plasmodium infection in mice. Eur J Immunol 47(4):685-691 |
| abstractText | gammadelta T cells play a crucial role in controlling malaria parasites. Dendritic cell (DC) activation via CD40 ligand (CD40L)-CD40 signaling by gammadelta T cells induces protective immunity against the blood-stage Plasmodium berghei XAT (PbXAT) parasites in mice. However, it is unknown which gammadelta T-cell subset has an effector role and is required to control the Plasmodium infection. Here, using antibodies to deplete TCR Vgamma1+ cells, we saw that Vgamma1+ gammadelta T cells were important for the control of PbXAT infection. Splenic Vgamma1+ gammadelta T cells preferentially expand and express CD40L, and both Vgamma1+ and Vgamma4+ gammadelta T cells produce IFN-gamma during infection. Although expression of CD40L on Vgamma1+ gammadelta T cells is maintained during infection, the IFN-gamma positivity of Vgamma1+ gammadelta T cells is reduced in late-phase infection due to gammadelta T-cell dysfunction. In Plasmodium-infected IFN-gamma signaling-deficient mice, DC activation is reduced, resulting in the suppression of gammadelta T-cell dysfunction and the dampening of gammadelta T-cell expansion in the late phase of infection. Our data suggest that Vgamma1+ gammadelta T cells represent a major subset responding to PbXAT infection and that the Vgamma1+ gammadelta T-cell response is dependent on IFN-gamma-activated DCs. |
