Interleukin (IL)-18 promotes the development of chronic gastrointestinal helminth infection by downregulating IL-13.
Interleukin (IL)-18 promotes the development of chronic gastrointestinal helminth infection by downregulating IL-13.
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DOI:
10.1084/jem.194.3.355
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发表时间:
2001-08-06
期刊:
影响因子:
--
通讯作者:
Grencis RK
中科院分区:
文献类型:
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作者:
Helmby H;Takeda K;Akira S;Grencis RK
Expulsion of the gastrointestinal nematode Trichuris muris is mediated by a T helper (Th) 2 type response involving interleukin (IL)-4 and IL-13. Here we show that Th1 response–associated susceptibility involves prior activation of IL-18 and caspase-1 followed by IL-12 and interferon (IFN)-γ in the intestine. IL-18–deficient mice are highly resistant to chronic T. muris infection and in vivo treatment of normal mice with recombinant (r)IL-18 suppresses IL-13 and IL-4 secretion but does not affect IFN-γ. In vivo treatment of T. muris–infected IFN-γ–deficient mice with rIL-18 demonstrated that the inhibitory effect of IL-18 on IL-13 secretion is independent of IFN-γ. Hence, IL-18 does not function as an IFN-γ–inducing cytokine during chronic T. muris infection but rather as a direct regulator of Th2 cytokines. These results provide the first demonstration of the critical role of IL-18 in regulating Th cell responses during gastrointestinal nematode infection.
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影响因子:
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作者:
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通讯作者:
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期刊:
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DOI:
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发表时间:
1997-03-17
期刊:
The Journal of experimental medicine
影响因子:
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作者:
通讯作者:
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