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CRTAM Protects Against Intestinal Dysbiosis During Pathogenic Parasitic Infection by Enabling Th17 Maturation
The gastrointestinal tract hosts the largest collection of commensal microbes in the body. Infections at this site can cause significant perturbations in the microbiota, known as dysbiosis, that facilitate the expansion of pathobionts, and can elicit inappropriate immune responses that impair the in...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6614434/ https://www.ncbi.nlm.nih.gov/pubmed/31312200 http://dx.doi.org/10.3389/fimmu.2019.01423 |
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author | Cervantes-Barragan, Luisa Cortez, Victor S. Wang, Qiuling McDonald, Keely G. Chai, Jiani N. Di Luccia, Blanda Gilfillan, Susan Hsieh, Chyi-Song Newberry, Rodney D. Sibley, L. David Colonna, Marco |
author_facet | Cervantes-Barragan, Luisa Cortez, Victor S. Wang, Qiuling McDonald, Keely G. Chai, Jiani N. Di Luccia, Blanda Gilfillan, Susan Hsieh, Chyi-Song Newberry, Rodney D. Sibley, L. David Colonna, Marco |
author_sort | Cervantes-Barragan, Luisa |
collection | PubMed |
description | The gastrointestinal tract hosts the largest collection of commensal microbes in the body. Infections at this site can cause significant perturbations in the microbiota, known as dysbiosis, that facilitate the expansion of pathobionts, and can elicit inappropriate immune responses that impair the intestinal barrier function. Dysbiosis typically occurs during intestinal infection with Toxoplasma gondii. Host resistance to T. gondii depends on a potent Th1 response. In addition, a Th17 response is also elicited. How Th17 cells contribute to the host response to T. gondii remains unclear. Here we show that class I-restricted T cell-associated molecule (CRTAM) expression on T cells is required for an optimal IL-17 production during T. gondii infection. Moreover, that the lack of IL-17, results in increased immunopathology caused by an impaired antimicrobial peptide production and bacterial translocation from the intestinal lumen to the mesenteric lymph nodes and spleen. |
format | Online Article Text |
id | pubmed-6614434 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-66144342019-07-16 CRTAM Protects Against Intestinal Dysbiosis During Pathogenic Parasitic Infection by Enabling Th17 Maturation Cervantes-Barragan, Luisa Cortez, Victor S. Wang, Qiuling McDonald, Keely G. Chai, Jiani N. Di Luccia, Blanda Gilfillan, Susan Hsieh, Chyi-Song Newberry, Rodney D. Sibley, L. David Colonna, Marco Front Immunol Immunology The gastrointestinal tract hosts the largest collection of commensal microbes in the body. Infections at this site can cause significant perturbations in the microbiota, known as dysbiosis, that facilitate the expansion of pathobionts, and can elicit inappropriate immune responses that impair the intestinal barrier function. Dysbiosis typically occurs during intestinal infection with Toxoplasma gondii. Host resistance to T. gondii depends on a potent Th1 response. In addition, a Th17 response is also elicited. How Th17 cells contribute to the host response to T. gondii remains unclear. Here we show that class I-restricted T cell-associated molecule (CRTAM) expression on T cells is required for an optimal IL-17 production during T. gondii infection. Moreover, that the lack of IL-17, results in increased immunopathology caused by an impaired antimicrobial peptide production and bacterial translocation from the intestinal lumen to the mesenteric lymph nodes and spleen. Frontiers Media S.A. 2019-07-02 /pmc/articles/PMC6614434/ /pubmed/31312200 http://dx.doi.org/10.3389/fimmu.2019.01423 Text en Copyright © 2019 Cervantes-Barragan, Cortez, Wang, McDonald, Chai, Di Luccia, Gilfillan, Hsieh, Newberry, Sibley and Colonna. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Immunology Cervantes-Barragan, Luisa Cortez, Victor S. Wang, Qiuling McDonald, Keely G. Chai, Jiani N. Di Luccia, Blanda Gilfillan, Susan Hsieh, Chyi-Song Newberry, Rodney D. Sibley, L. David Colonna, Marco CRTAM Protects Against Intestinal Dysbiosis During Pathogenic Parasitic Infection by Enabling Th17 Maturation |
title | CRTAM Protects Against Intestinal Dysbiosis During Pathogenic Parasitic Infection by Enabling Th17 Maturation |
title_full | CRTAM Protects Against Intestinal Dysbiosis During Pathogenic Parasitic Infection by Enabling Th17 Maturation |
title_fullStr | CRTAM Protects Against Intestinal Dysbiosis During Pathogenic Parasitic Infection by Enabling Th17 Maturation |
title_full_unstemmed | CRTAM Protects Against Intestinal Dysbiosis During Pathogenic Parasitic Infection by Enabling Th17 Maturation |
title_short | CRTAM Protects Against Intestinal Dysbiosis During Pathogenic Parasitic Infection by Enabling Th17 Maturation |
title_sort | crtam protects against intestinal dysbiosis during pathogenic parasitic infection by enabling th17 maturation |
topic | Immunology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6614434/ https://www.ncbi.nlm.nih.gov/pubmed/31312200 http://dx.doi.org/10.3389/fimmu.2019.01423 |
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