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2型免疫由固有免疫系统中造血非嗜酸性粒细胞的IL-4/IL-13表达所调控。

Type 2 immunity is controlled by IL-4/IL-13 expression in hematopoietic non-eosinophil cells of the innate immune system.

作者信息

Voehringer David, Reese Tiffany A, Huang Xiaozhu, Shinkai Kanade, Locksley Richard M

机构信息

Howard Hughes Medical Institute, Departments of Medicine and Microbiology/Immunology, University of California San Francisco, San Francisco, CA 94143, USA.

出版信息

J Exp Med. 2006 Jun 12;203(6):1435-46. doi: 10.1084/jem.20052448. Epub 2006 May 15.

DOI:10.1084/jem.20052448
PMID:16702603
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2118302/
Abstract

Nippostrongylus brasiliensis infection and ovalbumin-induced allergic lung pathology are highly interleukin (IL)-4/IL-13 dependent, but the contributions of IL-4/IL-13 from adaptive (T helper [Th]2 cells) and innate (eosinophil, basophils, and mast cells) immune cells remain unknown. Although required for immunoglobulin (Ig)E induction, IL-4/IL-13 from Th2 cells was not required for worm expulsion, tissue inflammation, or airway hyperreactivity. In contrast, innate hematopoietic cell-derived IL-4/IL-13 was dispensable for Th2 cell differentiation in lymph nodes but required for effector cell recruitment and tissue responses. Eosinophils were not required for primary immune responses. Thus, components of type 2 immunity mediated by IL-4/IL-13 are partitioned between T cell-dependent IgE and an innate non-eosinophil tissue component, suggesting new strategies for interventions in allergic immunity.

摘要

巴西日圆线虫感染和卵清蛋白诱导的过敏性肺部病理高度依赖白细胞介素(IL)-4/IL-13,但适应性(辅助性T [Th]2细胞)和先天性(嗜酸性粒细胞、嗜碱性粒细胞和肥大细胞)免疫细胞产生的IL-4/IL-13的作用仍不清楚。虽然Th2细胞产生的IL-4/IL-13是诱导免疫球蛋白(Ig)E所必需的,但蠕虫排出、组织炎症或气道高反应性并不需要它。相反,先天性造血细胞衍生的IL-4/IL-13在淋巴结中对Th2细胞分化并非必需,但对效应细胞募集和组织反应是必需的。嗜酸性粒细胞对初次免疫反应并非必需。因此,由IL-4/IL-13介导的2型免疫成分在T细胞依赖性IgE和先天性非嗜酸性粒细胞组织成分之间分配,这提示了干预过敏性免疫的新策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e619/2118302/7d62041257cf/jem2031435f07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e619/2118302/1fb221f15256/jem2031435f01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e619/2118302/91cae98106ce/jem2031435f02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e619/2118302/481e024a5c91/jem2031435f03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e619/2118302/919bd59400bf/jem2031435f04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e619/2118302/9164829cfab1/jem2031435f05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e619/2118302/cc8380aba018/jem2031435f06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e619/2118302/7d62041257cf/jem2031435f07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e619/2118302/1fb221f15256/jem2031435f01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e619/2118302/91cae98106ce/jem2031435f02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e619/2118302/481e024a5c91/jem2031435f03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e619/2118302/919bd59400bf/jem2031435f04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e619/2118302/9164829cfab1/jem2031435f05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e619/2118302/cc8380aba018/jem2031435f06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e619/2118302/7d62041257cf/jem2031435f07.jpg

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