期刊
IMMUNITY
卷 36, 期 5, 页码 821-833出版社
CELL PRESS
DOI: 10.1016/j.immuni.2012.03.021
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资金
- National Institutes of Health [RO1HL098935-01A1, AI080908]
- Sandler award for asthma [09-0035]
- Medical Research Council [MC_U105178805] Funding Source: researchfish
- MRC [MC_U105178805] Funding Source: UKRI
Interleukin-25 (IL-25 or IL-17E), a member of the structurally related 11,17 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(-)c-Kit(+) 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(-)c-Kit(+) 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(-)c-Kit(+) innate cell population through the positive-feedback loop of IL-25, initiating the type 2 immunity against helminth infection.
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