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Retinoic acid expression associates with enhanced IL-22 production by γδ T cells and innate lymphoid cells and attenuation of intestinal inflammation
Retinoic acid (RA), a vitamin A metabolite, modulates mucosal T helper cell responses. Here we examined the role of RA in regulating IL-22 production by γδ T cells and innate lymphoid cells in intestinal inflammation. RA significantly enhanced IL-22 production by γδ T cells stimulated in vitro with...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Rockefeller University Press
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3674702/ https://www.ncbi.nlm.nih.gov/pubmed/23690441 http://dx.doi.org/10.1084/jem.20121588 |
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author | Mielke, Lisa A. Jones, Sarah A. Raverdeau, Mathilde Higgs, Rowan Stefanska, Anna Groom, Joanna R. Misiak, Alicja Dungan, Lara S. Sutton, Caroline E. Streubel, Gundula Bracken, Adrian P. Mills, Kingston H.G. |
author_facet | Mielke, Lisa A. Jones, Sarah A. Raverdeau, Mathilde Higgs, Rowan Stefanska, Anna Groom, Joanna R. Misiak, Alicja Dungan, Lara S. Sutton, Caroline E. Streubel, Gundula Bracken, Adrian P. Mills, Kingston H.G. |
author_sort | Mielke, Lisa A. |
collection | PubMed |
description | Retinoic acid (RA), a vitamin A metabolite, modulates mucosal T helper cell responses. Here we examined the role of RA in regulating IL-22 production by γδ T cells and innate lymphoid cells in intestinal inflammation. RA significantly enhanced IL-22 production by γδ T cells stimulated in vitro with IL-1β or IL-18 and IL-23. In vivo RA attenuated colon inflammation induced by dextran sodium sulfate treatment or Citrobacter rodentium infection. This was associated with a significant increase in IL-22 secretion by γδ T cells and innate lymphoid cells. In addition, RA treatment enhanced production of the IL-22–responsive antimicrobial peptides Reg3β and Reg3γ in the colon. The attenuating effects of RA on colitis were reversed by treatment with an anti–IL-22 neutralizing antibody, demonstrating that RA mediates protection by enhancing IL-22 production. To define the molecular events involved, we used chromatin immunoprecipitation assays and found that RA promoted binding of RA receptor to the IL-22 promoter in γδ T cells. Our findings provide novel insights into the molecular events controlling IL-22 transcription and suggest that one key outcome of RA signaling may be to shape early intestinal immune responses by promoting IL-22 synthesis by γδ T cells and innate lymphoid cells. |
format | Online Article Text |
id | pubmed-3674702 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-36747022013-12-03 Retinoic acid expression associates with enhanced IL-22 production by γδ T cells and innate lymphoid cells and attenuation of intestinal inflammation Mielke, Lisa A. Jones, Sarah A. Raverdeau, Mathilde Higgs, Rowan Stefanska, Anna Groom, Joanna R. Misiak, Alicja Dungan, Lara S. Sutton, Caroline E. Streubel, Gundula Bracken, Adrian P. Mills, Kingston H.G. J Exp Med Brief Definitive Report Retinoic acid (RA), a vitamin A metabolite, modulates mucosal T helper cell responses. Here we examined the role of RA in regulating IL-22 production by γδ T cells and innate lymphoid cells in intestinal inflammation. RA significantly enhanced IL-22 production by γδ T cells stimulated in vitro with IL-1β or IL-18 and IL-23. In vivo RA attenuated colon inflammation induced by dextran sodium sulfate treatment or Citrobacter rodentium infection. This was associated with a significant increase in IL-22 secretion by γδ T cells and innate lymphoid cells. In addition, RA treatment enhanced production of the IL-22–responsive antimicrobial peptides Reg3β and Reg3γ in the colon. The attenuating effects of RA on colitis were reversed by treatment with an anti–IL-22 neutralizing antibody, demonstrating that RA mediates protection by enhancing IL-22 production. To define the molecular events involved, we used chromatin immunoprecipitation assays and found that RA promoted binding of RA receptor to the IL-22 promoter in γδ T cells. Our findings provide novel insights into the molecular events controlling IL-22 transcription and suggest that one key outcome of RA signaling may be to shape early intestinal immune responses by promoting IL-22 synthesis by γδ T cells and innate lymphoid cells. The Rockefeller University Press 2013-06-03 /pmc/articles/PMC3674702/ /pubmed/23690441 http://dx.doi.org/10.1084/jem.20121588 Text en © 2013 Mielke et al. 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 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/). |
spellingShingle | Brief Definitive Report Mielke, Lisa A. Jones, Sarah A. Raverdeau, Mathilde Higgs, Rowan Stefanska, Anna Groom, Joanna R. Misiak, Alicja Dungan, Lara S. Sutton, Caroline E. Streubel, Gundula Bracken, Adrian P. Mills, Kingston H.G. Retinoic acid expression associates with enhanced IL-22 production by γδ T cells and innate lymphoid cells and attenuation of intestinal inflammation |
title | Retinoic acid expression associates with enhanced IL-22 production by γδ T cells and innate lymphoid cells and attenuation of intestinal inflammation |
title_full | Retinoic acid expression associates with enhanced IL-22 production by γδ T cells and innate lymphoid cells and attenuation of intestinal inflammation |
title_fullStr | Retinoic acid expression associates with enhanced IL-22 production by γδ T cells and innate lymphoid cells and attenuation of intestinal inflammation |
title_full_unstemmed | Retinoic acid expression associates with enhanced IL-22 production by γδ T cells and innate lymphoid cells and attenuation of intestinal inflammation |
title_short | Retinoic acid expression associates with enhanced IL-22 production by γδ T cells and innate lymphoid cells and attenuation of intestinal inflammation |
title_sort | retinoic acid expression associates with enhanced il-22 production by γδ t cells and innate lymphoid cells and attenuation of intestinal inflammation |
topic | Brief Definitive Report |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3674702/ https://www.ncbi.nlm.nih.gov/pubmed/23690441 http://dx.doi.org/10.1084/jem.20121588 |
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