| First Author | Wakil AE | Year | 1998 |
| Journal | J Exp Med | Volume | 188 |
| Issue | 9 | Pages | 1651-6 |
| PubMed ID | 9802977 | Mgi Jnum | J:50765 |
| Mgi Id | MGI:1309703 | Doi | 10.1084/jem.188.9.1651 |
| Citation | Wakil AE, et al. (1998) Interferon gamma derived from CD4(+) T cells is sufficient to mediate T helper cell type 1 development. J Exp Med 188(9):1651-6 |
| abstractText | Interferon gamma (IFN-gamma) has been implicated in T helper type 1 (Th1) cell development through its ability to optimize interleukin 12 (IL-12) production from macrophages and IL-12 receptor expression on activated T cells. Various systems have suggested a role for IFN-gamma derived from the innate immune system, particularly natural killer (NK) cells, in mediating Th1 differentiation in vivo. We tested this requirement by reconstituting T cell and IFN-gamma doubly deficient mice with wild-type CD4(+) T cells and challenging the mice with pathogens that elicited either minimal or robust IL-12 in vivo (Leishmania major or Listeria monocytogenes, respectively). Th1 cells developed under both conditions, and this was unaffected by the presence or absence of IFN-gamma in non-T cells. Reconstitution with IFN-gamma-deficient CD4(+) T cells could not reestablish control over L. major, even in the presence of IFN-gamma from the NK compartment. These data demonstrate that activated T cells can maintain responsiveness to IL-12 through elaboration of endogenous IFN-gamma without requirement for an exogenous source of this cytokine. |
