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CUTTING EDGE |
-Chain (c) Reveals an Unexpected Role for CD4+ T Lymphocytes in Early IFN--Dependent Resistance to Toxoplasma gondii
*
Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, and
Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892
Mice lacking the common cytokine receptor 
-chain
(c) gene exhibit defective development of NK cells
and CD8+ T cells and greatly diminished production of
IFN-. Because resistance of SCID mice to Toxoplasma
gondii requires IL-12-dependent IFN- production by NK cells,
we expected that c-deficient mice would succumb rapidly
to the parasite. Surprisingly, however, most c-deficient
mice survived the acute phase of T. gondii infection. As in
wild-type mice, this resistance required IL-12 and IFN-;
nevertheless, whereas wild-type mice depleted of CD4+ T
cells survived, anti-CD4+ treated
c-deficient mice displayed diminished production of
IFN- and all succumbed to acute infection. These data not only
reveal a role for CD4+ T lymphocytes in IFN--dependent
host defense but also establish SCID and c-deficient
mice as powerful complementary tools for assessing the function of NK
vs CD4+ T cells in immunopathophysiologic responses.
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