{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,3]],"date-time":"2026-04-03T05:47:50Z","timestamp":1775195270624,"version":"3.50.1"},"reference-count":77,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2013,8,1]],"date-time":"2013-08-01T00:00:00Z","timestamp":1375315200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2013,8,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Tuberculosis, caused by Mycobacterium tuberculosis, remains a leading cause of mortality and morbidity worldwide, causing \u223c1.4 million deaths per year. Key immune components for host protection during tuberculosis include the cytokines IL-12, IL-1, and TNF-\u03b1, as well as IFN-\u03b3 and CD4+ Th1 cells. However, immune factors determining whether individuals control infection or progress to active tuberculosis are incompletely understood. Excess amounts of type I IFN have been linked to exacerbated disease during tuberculosis in mouse models and to active disease in patients, suggesting tight regulation of this family of cytokines is critical to host resistance. In addition, the immunosuppressive cytokine IL-10 is known to inhibit the immune response to M. tuberculosis in murine models through the negative regulation of key proinflammatory cytokines and the subsequent Th1 response. We show in this study, using a combination of transcriptomic analysis, genetics, and pharmacological inhibitors, that the TPL-2\u2013ERK1\/2 signaling pathway is important in mediating host resistance to tuberculosis through negative regulation of type I IFN production. The TPL-2\u2013ERK1\/2 signaling pathway regulated production by macrophages of several cytokines important in the immune response to M. tuberculosis as well as regulating induction of a large number of additional genes, many in a type I IFN-dependent manner. In the absence of TPL-2 in vivo, excess type I IFN promoted IL-10 production and exacerbated disease. These findings describe an important regulatory mechanism for controlling tuberculosis and reveal mechanisms by which type I IFN may promote susceptibility to this important disease.<\/jats:p>","DOI":"10.4049\/jimmunol.1300146","type":"journal-article","created":{"date-parts":[[2013,7,11]],"date-time":"2013-07-11T00:40:06Z","timestamp":1373503206000},"page":"1732-1743","source":"Crossref","is-referenced-by-count":90,"title":["TPL-2\u2013ERK1\/2 Signaling Promotes Host Resistance against Intracellular Bacterial Infection by Negative Regulation of Type I IFN Production"],"prefix":"10.1093","volume":"191","author":[{"given":"Finlay W","family":"McNab","sequence":"first","affiliation":[{"name":"Division of Immunoregulation, Medical Research Council, National Institute for Medical Research , London NW7 1AA,","place":["United Kingdom"]}]},{"given":"John","family":"Ewbank","sequence":"additional","affiliation":[{"name":"Division of Immunoregulation, Medical Research Council, National Institute for Medical Research , London NW7 1AA,","place":["United Kingdom"]}]},{"given":"Ricardo","family":"Rajsbaum","sequence":"additional","affiliation":[{"name":"Division of Immunoregulation, Medical Research Council, National Institute for Medical Research , London NW7 1AA,","place":["United Kingdom"]},{"name":"Department of Microbiology, Mount Sinai School of Medicine , New York, NY 10029"}]},{"given":"Evangelos","family":"Stavropoulos","sequence":"additional","affiliation":[{"name":"Division of Immunoregulation, Medical Research Council, National Institute for Medical Research , London NW7 1AA,","place":["United Kingdom"]}]},{"given":"Anna","family":"Martirosyan","sequence":"additional","affiliation":[{"name":"Division of Immunoregulation, Medical Research Council, National Institute for Medical Research , London NW7 1AA,","place":["United Kingdom"]}]},{"given":"Paul S","family":"Redford","sequence":"additional","affiliation":[{"name":"Division of Immunoregulation, Medical Research Council, National Institute for Medical Research , London NW7 1AA,","place":["United Kingdom"]}]},{"given":"Xuemei","family":"Wu","sequence":"additional","affiliation":[{"name":"Division of Immunoregulation, Medical Research Council, National Institute for Medical Research , London NW7 1AA,","place":["United Kingdom"]}]},{"given":"Christine M","family":"Graham","sequence":"additional","affiliation":[{"name":"Division of Immunoregulation, Medical Research Council, National Institute for Medical Research , London NW7 1AA,","place":["United Kingdom"]}]},{"given":"Margarida","family":"Saraiva","sequence":"additional","affiliation":[{"name":"Life and Health Sciences Research Institute, School of Health Sciences, University of Minho , Braga, 4710-057,","place":["Portugal"]},{"name":"Life and Health Sciences Research Institute\/Biomaterials, Biodegradables and Biomimetics-PT Government Associate Laboratory , Braga\/Guimaraes 4710-057,","place":["Portugal"]}]},{"given":"Philip","family":"Tsichlis","sequence":"additional","affiliation":[{"name":"Molecular Oncology Research Institute, Tufts Medical Center , Boston, MA 02111"}]},{"given":"Damien","family":"Chaussabel","sequence":"additional","affiliation":[{"name":"Benaroya Research Institute , Seattle, WA 98101"},{"name":"Baylor Institute for Immunology Research, INSERM U-899 , Dallas, TX 75204"}]},{"given":"Steven C","family":"Ley","sequence":"additional","affiliation":[{"name":"Division of Immune Cell Biology, Medical Research Council, National Institute for Medical Research , London NW7 1AA,","place":["United Kingdom"]}]},{"given":"Anne","family":"O\u2019Garra","sequence":"additional","affiliation":[{"name":"Division of Immunoregulation, Medical Research Council, National Institute for Medical Research , London NW7 1AA,","place":["United Kingdom"]},{"name":"National Heart and Lung Institute, Faculty of Medicine, Imperial College London , London SW7 2AZ,","place":["United Kingdom"]}]}],"member":"286","published-online":{"date-parts":[[2013,8,15]]},"reference":[{"key":"2025032405184102500_r1","doi-asserted-by":"crossref","first-page":"1266","DOI":"10.1164\/rccm.201203-0494UP","article-title":"Update in tuberculosis and nontuberculous mycobacterial disease 2011","volume":"185","author":"Nahid","year":"2012","journal-title":"Am. 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