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Innate myeloid cell TNFR1 mediates first line defence against primary Mycobacterium tuberculosis infection.
TNF is crucial for controlling Mycobacterium tuberculosis infection and understanding how will help immunomodulating the host response. Here we assessed the contribution of TNFR1 pathway from innate myeloid versus T cells. We first established the prominent role of TNFR1 in haematopoietic cells for...
Autores principales: | , , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4773807/ https://www.ncbi.nlm.nih.gov/pubmed/26931771 http://dx.doi.org/10.1038/srep22454 |
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author | Segueni, Noria Benmerzoug, Sulayman Rose, Stéphanie Gauthier, Amandine Bourigault, Marie-Laure Reverchon, Flora Philippeau, Amandine Erard, François Le Bert, Marc Bouscayrol, Hélène Wachter, Thierry Garcia, Irène Kollias, George Jacobs, Muazzam Ryffel, Bernhard Quesniaux, Valerie F.J. |
author_facet | Segueni, Noria Benmerzoug, Sulayman Rose, Stéphanie Gauthier, Amandine Bourigault, Marie-Laure Reverchon, Flora Philippeau, Amandine Erard, François Le Bert, Marc Bouscayrol, Hélène Wachter, Thierry Garcia, Irène Kollias, George Jacobs, Muazzam Ryffel, Bernhard Quesniaux, Valerie F.J. |
author_sort | Segueni, Noria |
collection | PubMed |
description | TNF is crucial for controlling Mycobacterium tuberculosis infection and understanding how will help immunomodulating the host response. Here we assessed the contribution of TNFR1 pathway from innate myeloid versus T cells. We first established the prominent role of TNFR1 in haematopoietic cells for controlling M. tuberculosis in TNFR1 KO chimera mice. Further, absence of TNFR1 specifically on myeloid cells (M-TNFR1 KO) recapitulated the uncontrolled M. tuberculosis infection seen in fully TNFR1 deficient mice, with increased bacterial burden, exacerbated lung inflammation, and rapid death. Pulmonary IL-12p40 over-expression was attributed to a prominent CD11b(+) Gr1(high) cell population in infected M-TNFR1 KO mice. By contrast, absence of TNFR1 on T-cells did not compromise the control of M. tuberculosis infection over 6-months. Thus, the protective TNF/TNFR1 pathway essential for controlling primary M. tuberculosis infection depends on innate macrophage and neutrophil myeloid cells, while TNFR1 pathway in T cells is dispensable. |
format | Online Article Text |
id | pubmed-4773807 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-47738072016-03-09 Innate myeloid cell TNFR1 mediates first line defence against primary Mycobacterium tuberculosis infection. Segueni, Noria Benmerzoug, Sulayman Rose, Stéphanie Gauthier, Amandine Bourigault, Marie-Laure Reverchon, Flora Philippeau, Amandine Erard, François Le Bert, Marc Bouscayrol, Hélène Wachter, Thierry Garcia, Irène Kollias, George Jacobs, Muazzam Ryffel, Bernhard Quesniaux, Valerie F.J. Sci Rep Article TNF is crucial for controlling Mycobacterium tuberculosis infection and understanding how will help immunomodulating the host response. Here we assessed the contribution of TNFR1 pathway from innate myeloid versus T cells. We first established the prominent role of TNFR1 in haematopoietic cells for controlling M. tuberculosis in TNFR1 KO chimera mice. Further, absence of TNFR1 specifically on myeloid cells (M-TNFR1 KO) recapitulated the uncontrolled M. tuberculosis infection seen in fully TNFR1 deficient mice, with increased bacterial burden, exacerbated lung inflammation, and rapid death. Pulmonary IL-12p40 over-expression was attributed to a prominent CD11b(+) Gr1(high) cell population in infected M-TNFR1 KO mice. By contrast, absence of TNFR1 on T-cells did not compromise the control of M. tuberculosis infection over 6-months. Thus, the protective TNF/TNFR1 pathway essential for controlling primary M. tuberculosis infection depends on innate macrophage and neutrophil myeloid cells, while TNFR1 pathway in T cells is dispensable. Nature Publishing Group 2016-03-02 /pmc/articles/PMC4773807/ /pubmed/26931771 http://dx.doi.org/10.1038/srep22454 Text en Copyright © 2016, Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Segueni, Noria Benmerzoug, Sulayman Rose, Stéphanie Gauthier, Amandine Bourigault, Marie-Laure Reverchon, Flora Philippeau, Amandine Erard, François Le Bert, Marc Bouscayrol, Hélène Wachter, Thierry Garcia, Irène Kollias, George Jacobs, Muazzam Ryffel, Bernhard Quesniaux, Valerie F.J. Innate myeloid cell TNFR1 mediates first line defence against primary Mycobacterium tuberculosis infection. |
title | Innate myeloid cell TNFR1 mediates first line defence against primary Mycobacterium
tuberculosis infection. |
title_full | Innate myeloid cell TNFR1 mediates first line defence against primary Mycobacterium
tuberculosis infection. |
title_fullStr | Innate myeloid cell TNFR1 mediates first line defence against primary Mycobacterium
tuberculosis infection. |
title_full_unstemmed | Innate myeloid cell TNFR1 mediates first line defence against primary Mycobacterium
tuberculosis infection. |
title_short | Innate myeloid cell TNFR1 mediates first line defence against primary Mycobacterium
tuberculosis infection. |
title_sort | innate myeloid cell tnfr1 mediates first line defence against primary mycobacterium
tuberculosis infection. |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4773807/ https://www.ncbi.nlm.nih.gov/pubmed/26931771 http://dx.doi.org/10.1038/srep22454 |
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