期刊
MUCOSAL IMMUNOLOGY
卷 8, 期 4, 页码 930-942出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/mi.2014.123
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资金
- NIH [R37 AI045898, R01 AI083450]
- CURED (Campaign Urging Research for Eosinophilic Disease) Foundation
- Food Allergy Research & Education (FARE)
- Buckeye Foundation
- Basic Science Research Program through the National Research Foundation of Korea - Ministry of Education [2013R1A1A2004820]
- Institute for Basic Science (IBS), Republic of Korea
- Grants-in-Aid for Scientific Research [24111005, 24111001] Funding Source: KAKEN
- Ministry of Science, ICT & Future Planning, Republic of Korea [IBS-R005-D1-2015-A00] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
- National Research Foundation of Korea [2013R1A1A2004820] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Eosinophils are multifunctional leukocytes that reside in the gastrointestinal (GI) lamina propria, where their basal function remains largely unexplored. In this study, by examining mice with a selective deficiency of systemic eosinophils (by lineage ablation) or GI eosinophils (eotaxin-1/2 double deficient orCC chemokine receptor 3 deficient), we show that eosinophils support immunoglobulin A (IgA) class switching, maintain intestinal mucus secretions, affect intestinal microbial composition, and promote the development of Peyer's patches. Eosinophil-deficient mice showed reduced expression of mediators of secretory IgA production, including intestinal interleukin 1 beta (IL-1 beta), inducible nitric oxide synthase, lymphotoxin (LT) alpha, and LT-beta, and reduced levels of retinoic acid-related orphan receptor gamma t-positive (ROR-gamma t(+)) innate lymphoid cells (ILCs), while maintaining normal levels of APRIL (a proliferation-inducing ligand), BAFF (B cell-activating factor of the tumor necrosis factor family), and TGF-beta (transforming growth factor beta). GI eosinophils expressed a relatively high level of IL-1 beta, and IL-1 beta-deficient mice manifested the altered gene expression profiles observed in eosinophil-deficient mice and decreased levels of IgA(+) cells and ROR-gamma t(+) ILCs. On the basis of these collective data, we propose that eosinophils are required for homeostatic intestinal immune responses including IgA production and that their affect is mediated via IL-1 beta in the small intestine.
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