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and IL-4 Responses to Viral Infections: Requirements for IL-21
Departments of
*
Molecular Microbiology and Immunology and
Medicine, Division of Biology and Medicine, Brown University, Providence, RI 02912; and
Emory Vaccine Center, Emory University, Atlanta, GA 30322
Cytokine responses to lymphocytic choriomeningitis virus infections
were evaluated, and CD8+ T cell, CD4+ T
cell, and IL-2 contributions delineated. In immunocompetent mice,
lymphocytic choriomeningitis virus induced both IFN-
and IL-4 as
well as IL-2. Experiments in mice either
ß2-microglobulin-deficient, lacking MHC class I molecules
and CD8+ T cells, or Aßb-deficient, lacking
MHC class II molecules and CD4+ T cells, demonstrated that
mixtures of T cell responses were required for optimal ex vivo cytokine
productions. Intracellular cytokine expression analyses of cells from
immunocompetent and immunodeficient mice showed that CD8+ T
cells were predominant IFN- producers, and that expansion of
CD8+ T cells primed to make IFN- was independent of
CD4+ T cells in vivo. Studies in IL-2-deficient mice
demonstrated that this cytokine promoted IFN- and IL-4 responses,
and ex vivo experiments showed that exogenous IL-2 was required to
maintain high-level IFN- production by in vivo-primed
CD8+ T cells. Conditions associated with cytokine decreases
were accompanied by reduced detectable plasma Ab responses. The results
indicate that, although IL-2-dependent CD8+ T cell
proliferation does not require endogenous CD4+ T cells,
IL-2 production by the CD4+ T cells may promote continued
cytokine release from activated CD8+ T cells. By defining
these critical steps in cellular and cytokine interactions for shaping
endogenous immune responses, the studies advance understanding of the
unique conditions regulating CD8+ T cell responses to viral
challenges.
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