期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 214, 期 6, 页码 1607-1618出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20160770
关键词
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资金
- Institute of Physical and Chemical Research
- Japan Society for the Promotion of Science KAKENHI [26460584, 25293114, 26116709, 26293111, 23229004, 24249029, 16H05207]
- Ministry of Education, Culture, Sports, Science and Technology KAKENHI [15H01165]
- Japan Agency for Medical Research and Development-Core Research for Evolutional Science and Technology [15652274]
- Japan Science and Technology Agency
- Uehara Memorial Foundation
- Naito Foundation Natural Science Scholarship
- Terumo Foundation for Life Sciences and Arts
- Grants-in-Aid for Scientific Research [15H01165, 17H01559, 25293114, 17H04089, 17KT0055, 26115007, 26293111, 16K14591, 16H05207] Funding Source: KAKEN
Interleukin-22 (IL-22) acts protectively and harmfully on intestinal tissue depending on the situation; therefore, IL-22 signaling needs to be tightly regulated. IL-22 binding protein (IL-22BP) binds IL-22 to inhibit IL-22 signaling. It is expressed in intestinal and lymphoid tissues, although its precise distribution and roles have remained unclear. In this study, we show that IL-22BP is highly expressed by CD11b(+)CD8 alpha(-) dendritic cells in the subepithelial dome region of Peyer's patches (PPs). We found that IL-22BP blocks IL-22 signaling in the follicle-associated epithelium (FAE) covering PPs, indicating that IL-22BP plays a role in regulating the characteristics of the FAE. As expected, FAE of IL-22BP-deficient (Il22ra2(-/-)) mice exhibited altered properties such as the enhanced expression of mucus and antimicrobial proteins as well as prominent fucosylation, which are normally suppressed in FAE. Additionally, Il22ra2(-/-) mice exhibited the decreased uptake of bacterial antigens into PPs without affecting M cell function. Our present study thus demonstrates that IL-22BP promotes bacterial uptake into PPs by influencing FAE gene expression and function.
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