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IFITM proteins drive type 2 T helper cell differentiation and exacerbate allergic airway inflammation.


ABSTRACT: The interferon-inducible transmembrane (Ifitm/Fragilis) genes encode homologous proteins that are induced by IFNs. Here, we show that IFITM proteins regulate murine CD4+ Th cell differentiation. Ifitm2 and Ifitm3 are expressed in wild-type (WT) CD4+ T cells. On activation, Ifitm3 was downregulated and Ifitm2 was upregulated. Resting Ifitm-family-deficient CD4+ T cells had higher expression of Th1-associated genes than WT and purified naive Ifitm-family-deficient CD4+ T cells differentiated more efficiently to Th1, whereas Th2 differentiation was inhibited. Ifitm-family-deficient mice, but not Ifitm3-deficient mice, were less susceptible than WT to induction of allergic airways disease, with a weaker Th2 response and less severe disease and lower Il4 but higher Ifng expression and IL-27 secretion. Thus, the Ifitm family is important in adaptive immunity, influencing Th1/Th2 polarization, and Th2 immunopathology.

SUBMITTER: Yanez DC 

PROVIDER: S-EPMC6396086 | biostudies-literature | 2019 Jan

REPOSITORIES: biostudies-literature

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The interferon-inducible transmembrane (Ifitm/Fragilis) genes encode homologous proteins that are induced by IFNs. Here, we show that IFITM proteins regulate murine CD4<sup>+</sup> Th cell differentiation. Ifitm2 and Ifitm3 are expressed in wild-type (WT) CD4<sup>+</sup> T cells. On activation, Ifitm3 was downregulated and Ifitm2 was upregulated. Resting Ifitm-family-deficient CD4<sup>+</sup> T cells had higher expression of Th1-associated genes than WT and purified naive Ifitm-family-deficient  ...[more]

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