Cutting edge: Type I IFN reverses human Th2 commitment and stability by suppressing GATA3

Jonathan P. Huber, Hilario J. Ramos, Michelle A. Gill, J. David Farrar

Research output: Contribution to journalArticlepeer-review

113 Scopus citations


T helper 2 cells regulate inflammatory responses to helminth infections while also mediating pathological processes of asthma and allergy. IL-4 promotes Th2 development by inducing the expression of the GATA3 transcription factor, and the Th2 phenotype is stabilized by a GATA3-dependent autoregulatory loop. In this study, we found that type I IFN(IFN-α/β) blocked human Th2 development and inhibited cytokine secretion from committed Th2 cells. This negative regulatory pathway was operative in human but not mouse CD4+ T cells and was selective to type I IFN, as neither IFN-γ nor IL-12 mediated such inhibition. IFN-α/β blocked Th2 cytokine secretion through the inhibition of GATA3 during Th2 development and in fully committed Th2 cells. Ectopic expression of GATA3 via retrovirus did not overcome IFN-α/β - mediated inhibition of Th2 commitment. Thus, we demonstrate a novel role for IFN-α/β in blocking Th2 cells, suggesting its potential as a promising therapy for atopy and asthma.

Original languageEnglish
Pages (from-to)813-817
Number of pages5
JournalJournal of Immunology
Issue number2
StatePublished - Jul 15 2010


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