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

IFITM proteins drive type 2 T helper cell differentiation and exacerbate allergic airway inflammation.
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IFITM蛋白驱动2 T型辅助细胞分化和加剧过敏性气道炎症。

DOI:
10.1002/eji.201847692
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发表时间:
2019-01
影响因子:
5.4
通讯作者:
Crompton T
Crompton T
中科院分区:
医学3区
文献类型:
--
作者:
Yánez DC;Sahni H;Ross S;Solanki A;Lau CI;Papaioannou E;Barbarulo A;Powell R;Lange UC;Adams DJ;Barenco M;Ono M;D'Acquisto F;Furmanski AL;Crompton T

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干扰素诱导的跨膜(IFITM/Fragilis)基因编码由IFN诱导的同源蛋白。在这里,我们展示了IFITM蛋白调节小鼠CD4+Th细胞分化。IFITM2和IFITM3在野生型(WT)CD4+T细胞中表达。在激活过程中,IFITM3下调,IFITM2上调。静息Ifit m家族缺陷的CD4+T细胞的Th1相关基因的表达高于WT,纯化的单纯Ifit m家族缺陷的CD4+T细胞更有效地分化为Th1,而Th2分化被抑制。IFITM家族缺陷小鼠,而不是IFITM3缺陷小鼠,比WT更不容易诱发过敏性呼吸道疾病,Th2反应较弱,疾病较轻,IL4较低,但IFNG表达和IL-27分泌较高。因此,IFIM家族在获得性免疫中起重要作用,影响Th1/Th2极化和Th2免疫病理。
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.
DOI: 10.1242/jcs.165803
发表时间: 2015-06-01
影响因子: 4
作者:
Furmanski AL;Barbarulo A;Solanki A;Lau CI;Sahni H;Saldana JI;D'Acquisto F;Crompton T
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发表时间: 2011-03-10
影响因子: 3.7
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通讯作者: Luster AD