{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,18]],"date-time":"2026-03-18T17:47:11Z","timestamp":1773856031922,"version":"3.50.1"},"reference-count":72,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2025,3,6]],"date-time":"2025-03-06T00:00:00Z","timestamp":1741219200000},"content-version":"vor","delay-in-days":2805,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2017,7,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Tuberculosis (TB), caused by Mycobacterium tuberculosis infection, is a leading cause of mortality and morbidity, causing \u223c1.5 million deaths annually. CD4+ T cells and several cytokines, such as the Th1 cytokine IFN-\u03b3, are critical in the control of this infection. Conversely, the immunosuppressive cytokine IL-10 has been shown to dampen Th1 cell responses to M. tuberculosis infection impairing bacterial clearance. However, the critical cellular source of IL-10 during M. tuberculosis infection is still unknown. Using IL-10 reporter mice, we show in this article that during the first 14 d of M. tuberculosis infection, the predominant cells expressing IL-10 in the lung were Ly6C+ monocytes. However, after day 21 postinfection, IL-10\u2013expressing T cells were also highly represented. Notably, mice deficient in T cell\u2013derived IL-10, but not mice deficient in monocyte-derived IL-10, showed a significant reduction in lung bacterial loads during chronic M. tuberculosis infection compared with fully IL-10\u2013competent mice, indicating a major role for T cell\u2013derived IL-10 in TB susceptibility. IL-10\u2013expressing cells were detected among both CD4+ and CD8+ T cells, expressed high levels of CD44 and Tbet, and were able to coproduce IFN-\u03b3 and IL-10 upon ex vivo stimulation. Furthermore, during M. tuberculosis infection, Il10 expression in CD4+ T cells was partially regulated by both IL-27 and type I IFN signaling. Together, our data reveal that, despite the multiple immune sources of IL-10 during M. tuberculosis infection, activated effector T cells are the major source accounting for IL-10\u2013induced TB susceptibility.<\/jats:p>","DOI":"10.4049\/jimmunol.1601340","type":"journal-article","created":{"date-parts":[[2017,6,6]],"date-time":"2017-06-06T00:20:15Z","timestamp":1496708415000},"page":"613-623","source":"Crossref","is-referenced-by-count":107,"title":["T Cell\u2013Derived IL-10 Impairs Host Resistance to <i>Mycobacterium tuberculosis<\/i> Infection"],"prefix":"10.1093","volume":"199","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4817-8196","authenticated-orcid":false,"given":"L\u00facia","family":"Moreira-Teixeira","sequence":"first","affiliation":[{"name":"Laboratory of Immunoregulation and Infection, The Francis Crick Institute , London NW1 1AT,","place":["United Kingdom"]}]},{"given":"Paul S","family":"Redford","sequence":"additional","affiliation":[{"name":"Laboratory of Immunoregulation and Infection, The Francis Crick Institute , London NW1 1AT,","place":["United Kingdom"]}]},{"given":"Evangelos","family":"Stavropoulos","sequence":"additional","affiliation":[{"name":"Laboratory of Immunoregulation and Infection, The Francis Crick Institute , London NW1 1AT,","place":["United Kingdom"]}]},{"given":"Nico","family":"Ghilardi","sequence":"additional","affiliation":[{"name":"Department of Immunology, Genentech Inc. , South San Francisco, CA 94080"}]},{"given":"Craig L","family":"Maynard","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Alabama at Birmingham , Birmingham, AL 35294"}]},{"given":"Casey T","family":"Weaver","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Alabama at Birmingham , Birmingham, AL 35294"}]},{"given":"Ana Paula","family":"Freitas do Ros\u00e1rio","sequence":"additional","affiliation":[{"name":"Malaria Immunology Laboratory, The Francis Crick Institute , London NW1 1AT,","place":["United Kingdom"]}]},{"given":"Xuemei","family":"Wu","sequence":"additional","affiliation":[{"name":"Laboratory of Immunoregulation and Infection, The Francis Crick Institute , London NW1 1AT,","place":["United Kingdom"]}]},{"given":"Jean","family":"Langhorne","sequence":"additional","affiliation":[{"name":"Malaria Immunology Laboratory, The Francis Crick Institute , London NW1 1AT,","place":["United Kingdom"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9845-6134","authenticated-orcid":false,"given":"Anne","family":"O\u2019Garra","sequence":"additional","affiliation":[{"name":"Laboratory of Immunoregulation and Infection, The Francis Crick Institute , London NW1 1AT,","place":["United Kingdom"]},{"name":"National Heart and Lung Institute, Faculty of Medicine, Imperial College London , London SW3 6NP,","place":["United Kingdom"]}]}],"member":"286","published-online":{"date-parts":[[2017,7,15]]},"reference":[{"key":"2025030614184015500_r1","volume-title":"Global Tuberculosis Report 2015.","author":"WHO","year":"2015"},{"key":"2025030614184015500_r2","doi-asserted-by":"crossref","first-page":"93","DOI":"10.1146\/annurev.immunol.19.1.93","article-title":"Immunology of tuberculosis","volume":"19","author":"Flynn","year":"2001","journal-title":"Annu. 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