| First Author | Haring JS | Year | 2005 |
| Journal | J Immunol | Volume | 175 |
| Issue | 5 | Pages | 3117-22 |
| PubMed ID | 16116201 | Mgi Jnum | J:113254 |
| Mgi Id | MGI:3664853 | Doi | 10.4049/jimmunol.175.5.3117 |
| Citation | Haring JS, et al. (2005) In vivo generation of pathogen-specific Th1 cells in the absence of the IFN-gamma receptor. J Immunol 175(5):3117-22 |
| abstractText | The precise mechanisms that govern the commitment of CD4 T cells to become Th1 or Th2 cells in vivo are incompletely understood. Recent experiments demonstrate colocalization of the IFN-gammaR chains with the TCR during activation of naive CD4 T cells, suggesting that association of these molecules may be involved in determining lineage commitment. To test the role of IFN-gamma and its receptor in the generation of Th1 Ag-specific CD4 T cells, we analyzed mice after infection with Listeria monocytogenes or lymphocytic choriomeningitis virus. In the absence of IFN-gamma, Ag-specific CD4 T cells were generated in response to both these infections. In addition, IFN-gamma-producing (Th1) Ag-specific CD4 T cells were generated in mice lacking the ligand-binding chain of the IFN-gammaR (IFN-gammaR1-/-) or the signaling chain (IFN-gammaR2-/-). There was no increase in the number of IL-4-producing Ag-specific CD4 T cells, nor was there a decrease in the expression of T-bet in the absence of functional IFN-gamma signaling, indicating that the cells were committed Th1 cells. Thus, both chains of the IFN-gammaR are dispensable for the generation of Th1 Ag-specific CD4 T cells after infection in vivo. |
