Epithelial Cell-Specific Act1 Adaptor Mediates Interleukin-25-Dependent Helminth Expulsion through Expansion of Lin<sup>鈭?/sup>c-Kit<sup>+sup> Innate Cell Population

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• 作者：Zizhen Kang<sup>1sup> ; Shadi Swaidani<sup>1sup> ; Weiguo Yin<sup>1sup> ; Chenhui Wang<sup>1sup> ; Jillian  ; L. Barlow<sup>3sup> ; Muhammet  ; Fatih Gulen<sup>1sup> ; Katarzyna Bulek<sup>1sup> ; Jeong-su Do<sup>1sup> ; Mark Aronica<sup>2sup> ; Andrew  ; N.J. McKenzie<sup>3sup> ; Booki Min<sup>1sup> ; Xiaoxia Li<sup>1sup><sup> ; sup><sup>lix@ccf.orgsup>
• 刊名：Immunity
• 出版年：2012
• 期刊代码：40_10747613
• 类别：imm
• 出版时间：25 May, 2012
• 卷：36
• 期：5
• 页码：821-833
• 文件大小：1612 K

摘要

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ss="h3">Summary

Interleukin-25 (IL-25 or IL-17E), a member of the structurally related IL-17 family, functions as an important mediator of T helper 2 cell-type (type 2) responses. We examined the cell type-specific role of IL-25-induced Act1-mediated signaling in protective immunity against helminth infection. Targeted Act1 deficiency in epithelial cells resulted in a marked delay in worm expulsion and abolished the expansion of the Lin<sup>鈭?/sup>c-Kit<sup>+sup> innate cell population in the mesenteric lymph node, lung, and liver. Th2 cell-inducing cytokine (IL-25 and IL-33) expression were reduced in the intestinal epithelial cells from the infected and IL-25-injected epithelial-specific Act1-deficient mice. Adoptive transfer of Lin<sup>鈭?/sup>c-Kit<sup>+sup> cells or combined injection of IL-25 and IL-33 restored the type 2 responses in these mice. Taken together, these results suggest that epithelial-specific Act1 mediates the expansion of the Lin<sup>鈭?/sup>c-Kit<sup>+sup> innate cell population through the positive-feedback loop of IL-25, initiating the type 2 immunity against helminth infection.