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白细胞介素-18与白细胞介素-2共同作用，通过激活黏膜肥大细胞依赖性2型固有免疫来抵御委内瑞拉类圆线虫感染。

IL-18 with IL-2 protects against Strongyloides venezuelensis infection by activating mucosal mast cell-dependent type 2 innate immunity.

作者信息

Sasaki Yuki, Yoshimoto Tomohiro, Maruyama Haruhiko, Tegoshi Tatsuya, Ohta Nobuo, Arizono Naoki, Nakanishi Kenji

机构信息

Department of Immunology and Medical Zoology, Hyogo College of Medicine, Nishinomiya, Japan.

出版信息

J Exp Med. 2005 Sep 5;202(5):607-16. doi: 10.1084/jem.20042202. Epub 2005 Aug 29.

DOI:10.1084/jem.20042202
PMID:16129701
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2212862/
Abstract

C57BL/6 (B6) and B6 background STAT6(-/-) mice pretreated with IL-18 plus IL-2 showed prominent intestinal mastocytosis and rapidly expelled implanted adult worms of the gastrointestinal nematode Strongyloides venezuelensis. In contrast, identically pretreated mast cell-deficient W/W(v) mice failed to do so. Thus, activated mucosal mast cells (MMC) are crucial for parasite expulsion. B6 mice infected with S. venezuelensis third-stage larvae (L3) completed parasite expulsion by day 12 after infection, whereas IL-18(-/-) or IL-18Ralpha(-/-) B6 mice exhibited marked impairment in parasite expulsion, suggesting a substantial contribution of IL-18-dependent MMC activation to parasite expulsion. Compared with IL-18(-/-) or IL-18Ralpha(-/-) mice, S. venezuelensis L3-infected STAT6(-/-) mice have poorly activated MMC and sustained infection; although their IL-18 production is normal. Neutralization of IL-18 and IL-2 further reduces expulsion in infected STAT6(-/-) mice. These results suggest that collaboration between IL-18-dependent and Th2 cell-dependent mastocytosis is important for prompt parasite expulsion.

摘要

用白细胞介素-18（IL-18）加白细胞介素-2（IL-2）预处理的C57BL/6（B6）和B6背景的STAT6基因敲除小鼠表现出显著的肠道肥大细胞增多，并能迅速排出植入的胃肠道线虫委内瑞拉类圆线虫的成虫。相比之下，同样经过预处理的肥大细胞缺陷型W/W（v）小鼠则无法做到这一点。因此，活化的黏膜肥大细胞（MMC）对于寄生虫的排出至关重要。感染委内瑞拉类圆线虫第三期幼虫（L3）的B6小鼠在感染后第12天完成寄生虫排出，而IL-18基因敲除或IL-18受体α亚基（IL-18Rα）基因敲除的B6小鼠在寄生虫排出方面表现出明显受损，这表明依赖IL-18的MMC活化对寄生虫排出有重要贡献。与IL-18基因敲除或IL-18Rα基因敲除小鼠相比，感染委内瑞拉类圆线虫L3的STAT6基因敲除小鼠的MMC活化较差且感染持续存在；尽管它们的IL-18产生正常。中和IL-18和IL-2会进一步降低感染的STAT6基因敲除小鼠的寄生虫排出率。这些结果表明，依赖IL-18的和Th2细胞依赖的肥大细胞增多之间的协同作用对于迅速排出寄生虫很重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebfa/2212862/ae1ae8d3d6c8/20042202f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebfa/2212862/e1fcc2a7f2fe/20042202f1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebfa/2212862/b57163098efc/20042202f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebfa/2212862/542237977961/20042202f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebfa/2212862/fac9cec44e13/20042202f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebfa/2212862/ae1ae8d3d6c8/20042202f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebfa/2212862/e1fcc2a7f2fe/20042202f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebfa/2212862/3dbc65f868d1/20042202f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebfa/2212862/adab7abec878/20042202f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebfa/2212862/b57163098efc/20042202f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebfa/2212862/542237977961/20042202f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebfa/2212862/fac9cec44e13/20042202f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebfa/2212862/ae1ae8d3d6c8/20042202f7.jpg

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