Nature Immunology5, 1157 - 1165 (2004)
Published online: 10 October 2004; | doi:10.1038/ni1128
Conditional deletion of Gata3 shows its essential function in TH1-TH2 responses
Jinfang Zhu1, Booki Min1, Jane Hu-Li1, Cynthia J Watson1, Alex Grinberg4, Qi Wang2, Nigel Killeen2, Joseph F Urban Jr3, Liying Guo1
& William E Paul1
1
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.
2
Department of Microbiology and Immunology, University of California at San Francisco, San Francisco, California 94143, USA.
3
Nutrient Requirements and Functions Laboratory, Beltsville Human Nutrition Research Center, US Department of Agriculture, Beltsville, Maryland 20705, USA.
4
Laboratory of Mammalian Genes and Development, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892, USA.
Expression of the transcription factor GATA-3 is strongly associated with T helper type 2 (TH2) differentiation, but genetic evidence for its involvement in this process has been lacking. Here, we generated a conditional GATA-3-deficient mouse line. In vitro deletion of Gata3 diminished both interleukin 4 (IL-4)−dependent and IL-4-independent TH2 cell differentiation; without GATA-3, TH1 differentiation occurred in the absence of IL-12 and interferon-. Gata3 deletion limited the growth of TH2 cells but not TH1 cells. Deletion of Gata3 from established TH2 cells abolished IL-5 and IL-13 but not IL-4 production. In vivo deletion of Gata3 using OX40-Cre eliminated TH2 responses and allowed the development of interferon--producing cells in mice infected with Nippostrongylus brasiliensis. Thus, GATA-3 serves as a principal switch in determining TH1-TH2 responses.
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. Gata3 deletion limited the growth of TH2 cells but not TH1 cells. Deletion of Gata3 from established TH2 cells abolished IL-5 and IL-13 but not IL-4 production. In vivo deletion of Gata3 using OX40-Cre eliminated TH2 responses and allowed the development of interferon-
