A new aspect of IL-15 in mucosal immunity and inflammation.
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- YUKI Yoshikazu
- Division of Mucosal Immnonology, Department of Microbiology and Immunology, Institute of Medical Science, The University of Tokyo
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- OHTA Noriyuki
- Department of Mucosal Immunology, Research Institute for Microbial Diseases, Osaka University
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- HIROI Takachika
- Department of Mucosal Immunology, Research Institute for Microbial Diseases, Osaka University
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- KIYONO Hiroshi
- Division of Mucosal Immnonology, Department of Microbiology and Immunology, Institute of Medical Science, The University of Tokyo Department of Mucosal Immunology, Research Institute for Microbial Diseases, Osaka University
Bibliographic Information
- Other Title
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- 粘膜の生理と病態 IL‐15の粘膜免疫と炎症へのかかわり
- IL-15の粘膜免疫と炎症へのかかわり
- IL 15 ノ ネンマク メンエキ ト エンショウ エ ノ カカワリ
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Abstract
In this review, a new relationship between IL-15 and mucosal immunity/inflammation was discussed based on the results obtained by a novel IL-15-induced inflammatory bowel disease murine model. First, we provide new evidence that IL-15 is a critically important mucosal cytokine for the regulation of IgA responses. It has been shown that intestinal B-1 cells preferentially express IL-15R. Furthermore, it has been demonstrated that IL-15 acts on two different stages (sIgM− sIgA+ and sIgM+ sIgA−) of CMIS-independent B-1 cells development, while IL-5 only acts on the stage of sIgM− sIgA+ B-1 cells. In contrast, CMIS-dependent B-2 cells originating from IgA inductive sites (e.g., PP) express IL-5R and IL-6R, but not IL-15R, and can respond to stimulation signals provided by both IL-5 and IL-6 to become IgA-producing cells. Secondly, we have established a new model of small intestinal inflammation by selective overexpression of IL-15 in the murine gastrointestinal tract (T3b-IL-15 Tg mice). IL-15-induced CD8-alpha beta+ T cells expressing NK1.1 appear to be critical in the pathogenesis of the small intestinal lesions in the transgenic mice. Further more, this unique subset of CD8-alpha beta+ T cells preferentially produced Th-1-type cytokines, and the preferential expansion of these T cells could be attributed to the anti-apoptotic activity of IL-15. These results suggest that dysregulation of IL-15 results in deleterious effects for the host, in spite of it being a critically important mucosal cytokine for the regulation of IgA responses.<br>
Journal
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- Folia Pharmacologica Japonica
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Folia Pharmacologica Japonica 120 (1), 32-38, 2002
The Japanese Pharmacological Society
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Keywords
Details 詳細情報について
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- CRID
- 1390282679247514752
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- NII Article ID
- 10009512271
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- NII Book ID
- AN00198335
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- ISSN
- 13478397
- 00155691
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- NDL BIB ID
- 6205992
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- Text Lang
- ja
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- Data Source
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- JaLC
- NDL
- Crossref
- CiNii Articles
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- Abstract License Flag
- Disallowed