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CD11b facilitates the development of peripheral tolerance by suppressing Th17 differentiation
Antigen-induced immune suppression, like T cell activation, requires antigen-presenting cells (APCs); however, the role of APCs in mediating these opposing effects is not well understood, especially in vivo. We report that genetic inactivation of CD11b, which is a CD18 subfamily of integrin receptor...
Autores principales: | , , , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
The Rockefeller University Press
2007
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118631/ https://www.ncbi.nlm.nih.gov/pubmed/17562817 http://dx.doi.org/10.1084/jem.20062292 |
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author | Ehirchiou, Driss Xiong, Ying Xu, Guangwu Chen, Wanjun Shi, Yufang Zhang, Li |
author_facet | Ehirchiou, Driss Xiong, Ying Xu, Guangwu Chen, Wanjun Shi, Yufang Zhang, Li |
author_sort | Ehirchiou, Driss |
collection | PubMed |
description | Antigen-induced immune suppression, like T cell activation, requires antigen-presenting cells (APCs); however, the role of APCs in mediating these opposing effects is not well understood, especially in vivo. We report that genetic inactivation of CD11b, which is a CD18 subfamily of integrin receptors that is highly expressed on APCs, abolishes orally induced peripheral immune tolerance (oral tolerance) without compromising APC maturation or antigen-specific immune activation. The defective oral tolerance in CD11b(−/−) mice can be restored by adoptive transfer of wild-type APCs. CD11b deficiency leads to enhanced interleukin (IL) 6 production by APCs, which subsequently promotes preferential differentiation of naive T cells to T helper 17 (Th17) cells, which are a T cell lineage characterized by their production of IL-17. Consequently, antigen feeding and immunization of CD11b(−/−) mice results in significant production of IL-17 within the draining lymph nodes that interferes with the establishment of oral tolerance. Together, we conclude that CD11b facilitates oral tolerance by suppressing Th17 immune differentiation. |
format | Text |
id | pubmed-2118631 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2007 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21186312008-01-09 CD11b facilitates the development of peripheral tolerance by suppressing Th17 differentiation Ehirchiou, Driss Xiong, Ying Xu, Guangwu Chen, Wanjun Shi, Yufang Zhang, Li J Exp Med Brief Definitive Reports Antigen-induced immune suppression, like T cell activation, requires antigen-presenting cells (APCs); however, the role of APCs in mediating these opposing effects is not well understood, especially in vivo. We report that genetic inactivation of CD11b, which is a CD18 subfamily of integrin receptors that is highly expressed on APCs, abolishes orally induced peripheral immune tolerance (oral tolerance) without compromising APC maturation or antigen-specific immune activation. The defective oral tolerance in CD11b(−/−) mice can be restored by adoptive transfer of wild-type APCs. CD11b deficiency leads to enhanced interleukin (IL) 6 production by APCs, which subsequently promotes preferential differentiation of naive T cells to T helper 17 (Th17) cells, which are a T cell lineage characterized by their production of IL-17. Consequently, antigen feeding and immunization of CD11b(−/−) mice results in significant production of IL-17 within the draining lymph nodes that interferes with the establishment of oral tolerance. Together, we conclude that CD11b facilitates oral tolerance by suppressing Th17 immune differentiation. The Rockefeller University Press 2007-07-09 /pmc/articles/PMC2118631/ /pubmed/17562817 http://dx.doi.org/10.1084/jem.20062292 Text en Copyright © 2007, The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Brief Definitive Reports Ehirchiou, Driss Xiong, Ying Xu, Guangwu Chen, Wanjun Shi, Yufang Zhang, Li CD11b facilitates the development of peripheral tolerance by suppressing Th17 differentiation |
title | CD11b facilitates the development of peripheral tolerance by suppressing Th17 differentiation |
title_full | CD11b facilitates the development of peripheral tolerance by suppressing Th17 differentiation |
title_fullStr | CD11b facilitates the development of peripheral tolerance by suppressing Th17 differentiation |
title_full_unstemmed | CD11b facilitates the development of peripheral tolerance by suppressing Th17 differentiation |
title_short | CD11b facilitates the development of peripheral tolerance by suppressing Th17 differentiation |
title_sort | cd11b facilitates the development of peripheral tolerance by suppressing th17 differentiation |
topic | Brief Definitive Reports |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118631/ https://www.ncbi.nlm.nih.gov/pubmed/17562817 http://dx.doi.org/10.1084/jem.20062292 |
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