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In this study, we found that among pleural fluid (PF) lymphocytes, natural killer (NK) cells are a major source of early gamma interferon (IFN-\u03b3) upon<jats:italic>M. tuberculosis<\/jats:italic>stimulation, leading us to investigate the mechanisms and molecules involved in this process. We show that the whole bacterium is the best inducer of IFN-\u03b3, although a high-molecular-weight fraction of culture filtrate proteins from<jats:italic>M. tuberculosis<\/jats:italic>H37Rv and the whole-cell lysate also induce its expression. The mannose receptor seems to mediate the inhibitory effect of mannosylated lipoarabinomannan, and Toll-like receptor 2 and 4 agonists activate NK cells but do not induce IFN-\u03b3 like<jats:italic>M. tuberculosis<\/jats:italic>does. Antigen-presenting cells (APC) and NK cells bind<jats:italic>M. tuberculosis<\/jats:italic>, and although interleukin-12 is required, it is not sufficient to induce IFN-\u03b3 expression, indicating that NK cell-APC contact takes place. Indeed, major histocompatibility complex class I, adhesion, and costimulatory molecules as well as NK receptors regulate IFN-\u03b3 induction. The signaling pathway is partially inhibited by dexamethasone and sensitive to Ca<jats:sup>2+<\/jats:sup>flux and cyclosporine. Inhibition of p38 and extracellular-regulated kinase mitogen-activated protein kinase pathways reduces the number of IFN-\u03b3<jats:sup>+<\/jats:sup>NK cells. Phosphorylated p38 (p-p38) is detected in ex vivo PF-NK cells, and<jats:italic>M. tuberculosis<\/jats:italic>triggers p-p38 in PF-NK cells at the same time that binding between NK and<jats:italic>M. tuberculosis<\/jats:italic>reaches its maximum value. Thus, interplay between<jats:italic>M. tuberculosis<\/jats:italic>and NK cells\/APC triggering IFN-\u03b3 would be expected to play a beneficial role in tuberculous pleurisy by helping to maintain a type 1 profile.<\/jats:p>","DOI":"10.1128\/iai.00381-07","type":"journal-article","created":{"date-parts":[[2007,8,21]],"date-time":"2007-08-21T00:58:49Z","timestamp":1187657929000},"page":"5325-5337","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":55,"title":["<i>Mycobacterium tuberculosis<\/i>-Induced Gamma Interferon Production by Natural Killer Cells Requires Cross Talk with Antigen-Presenting Cells Involving Toll-Like Receptors 2 and 4 and the Mannose Receptor in Tuberculous Pleurisy"],"prefix":"10.1128","volume":"75","author":[{"given":"Pablo","family":"Schierloh","sequence":"first","affiliation":[{"name":"Departamento de Inmunologi\u0301a, Instituto de Investigaciones Hematolo\u0301gicas, Academia Nacional de Medicina"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Noemi\u0301","family":"Yokobori","sequence":"additional","affiliation":[{"name":"Departamento de Inmunologi\u0301a, Instituto de Investigaciones Hematolo\u0301gicas, Academia Nacional de Medicina"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mercedes","family":"Alema\u0301n","sequence":"additional","affiliation":[{"name":"Departamento de Inmunologi\u0301a, Instituto de Investigaciones Hematolo\u0301gicas, Academia Nacional de Medicina"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vero\u0301nica","family":"Landoni","sequence":"additional","affiliation":[{"name":"Departamento de Inmunologi\u0301a, Instituto de Investigaciones Hematolo\u0301gicas, Academia Nacional de Medicina"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laura","family":"Geffner","sequence":"additional","affiliation":[{"name":"Departamento de Inmunologi\u0301a, Instituto de Investigaciones Hematolo\u0301gicas, Academia Nacional de Medicina"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rosa M.","family":"Musella","sequence":"additional","affiliation":[{"name":"Divisio\u0301n de Tisioneumonologi\u0301a, Hospital F. 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