Type I IFN exacerbates disease in tuberculosis-susceptible mice by inducing neutrophil-mediated lung inflammation and NETosis

Type I IFN exacerbates disease in tuberculosis-susceptible mice by inducing neutrophil-mediated lung inflammation and NETosis

GM-CSF is involved in control over M. tuberculosis infection. Here the authors show that GM-CSF reduces type 1 interferon driven neutrophil recruitment, NETosis and bacterial growth in the lungs of infected mice, and provide evidence that this NETosis occurs in infected humans who are not responsive...

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Autores principales: Lúcia Moreira-Teixeira, Philippa J. Stimpson, Evangelos Stavropoulos, Sabelo Hadebe, Probir Chakravarty, Marianna Ioannou, Iker Valle Aramburu, Eleanor Herbert, Simon L. Priestnall, Alejandro Suarez-Bonnet, Jeremy Sousa, Kaori L. Fonseca, Qian Wang, Sergo Vashakidze, Paula Rodríguez-Martínez, Cristina Vilaplana, Margarida Saraiva, Venizelos Papayannopoulos, Anne O’Garra
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2020
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Science
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Acceso en línea:https://doaj.org/article/17bb66cf20aa478d882dee5a8fe9ffd3
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Sumario:GM-CSF is involved in control over M. tuberculosis infection. Here the authors show that GM-CSF reduces type 1 interferon driven neutrophil recruitment, NETosis and bacterial growth in the lungs of infected mice, and provide evidence that this NETosis occurs in infected humans who are not responsive to antibiotic therapy.

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