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Endogenous IFN‐γ and IL‐18 production directly limit induction of type 2 immunity in vivo

Allergic diseases are associated with excessive type 2 immunity, yet the endogenous controls — if any — responsible for limiting induction of such responses remain unclear. Using IL‐12‐deficient mice, we recently showed that endogenous IL‐12 is not essential for preventing development of allergic responses. Here, we examine the roles of endogenous IFN‐γ and IL‐18 production in limiting the occurrence and severity of type 2 immunity. Lack of endogenous IFN‐γ synthesis results in significantly higher type 2 cytokine (IL‐4, IL‐5, IL‐10 and IL‐13) and chemokine (TARC) production following exogenous antigen exposure. Thus, IFN‐γ, but not IL‐12, is a key negative regulator of the type 2 immune response. IL‐18, in addition to its established role as an inducer of IFN‐γ, also negatively regulates CD4+ T cell‐derived IL‐4 synthesis via an IFN‐γ‐independent mechanism, thereby further limiting the development of type 2 immune responses. Together, theseresults identify endogenous IFN‐γ and IL‐18 as potent, independent, negative regulators of the development of type 2 immunity to ubiquitous environmental antigens.