Description:
<jats:p>Viral infections trigger the production of type I interferon (IFNα/β) as well as Th1 cytokines like IL‐12 and IFNγ. In contrast, IFNα is not associated with Th2 responses, which are controlled by IL‐4. Hence, the effect of IFNα on Th2 development has not been very well characterized despite its importance for understanding how CD4<jats:sup>+</jats:sup> T cells respond to virus infections in Th2‐biased conditions like asthma. To address this issue, we studied the effects of IFNα on IL‐4‐dependent Th2 development in human CD4+ T cells. In these studies, we found that IFNα dominantly inhibits the ability of IL‐4 to promote Th2 differentiation. Further, this effect is specific to IFNα, as neither IL‐12 nor IFNγ inhibit IL‐4‐regulated Th2 development. IFNα inhibits Th2 development by blocking the induction of GATA‐3 independently of STAT6 activation. Thus, we have found a novel function of IFNα in the inhibition of Th2 responses that may be useful as a therapeutic approach to the treatment of asthma.</jats:p><jats:p>This study is supported by a grant from the NIH/NIAID (AI56222) and by a training grant from the NIH/NIAID (5T32AI005284).</jats:p>