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Articles |
Derived from CD4+ T Cells Is Sufficient to Mediate T Helper Cell Type 1 Development
Howard Hughes Medical Institute, University of California San Francisco, San Francisco, California 94143; and the Veterans Administration Medical Center, San Francisco, California 94121
Interferon
(IFN-) 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- 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- 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- in non-T cells. Reconstitution with IFN-–deficient CD4+ T cells could not reestablish control over L. major, even in the presence of IFN- from the NK compartment. These data demonstrate that activated T cells can maintain responsiveness to IL-12 through elaboration of endogenous IFN- without requirement for an exogenous source of this cytokine.
Key Words: T helper type 1 cells • interferon • natural killer cells • Leishmania • Listeria
Abbreviations used: RAG-1–/–, recombinase activating gene– deficient mice.
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