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In this study, we evaluated the immune function of Rv1737c, which is a latency\u2010associated antigen of dormancy survival regulator (DosR) of <jats:italic>M.\u00a0tuberculosis<\/jats:italic> in a mouse model. Our data showed that mice pretreated with recombinant Rv1737c (<jats:styled-content style=\"fixed-case\">rR<\/jats:styled-content>v1737c) exhibited higher levels of antigen\u2010specific antibodies (IgG, IgM and IgA) than sham\u2010treated mice. Following Bacilli Calmette\u2010Guerin (<jats:styled-content style=\"fixed-case\">BCG<\/jats:styled-content>) challenge, <jats:styled-content style=\"fixed-case\">rR<\/jats:styled-content>v1737c adjuvanted with cholera toxin subunit B (<jats:styled-content style=\"fixed-case\">CTB<\/jats:styled-content>) induced diffuse lung inflammation and fibrosis compared to the control mice. The inflammatory pathogenesis due to <jats:styled-content style=\"fixed-case\">rR<\/jats:styled-content>v1737c pre\u2010exposure was associated with a switch in the macrophage phenotype from M1 to activated M2 and was characterized by <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201010 production. Intracellular cytokine analysis further showed that the <jats:styled-content style=\"fixed-case\">rR<\/jats:styled-content>v1737c\u2010pretreated mice exhibited an increased frequency of Th2 cells in the lungs, lymph nodes and spleen after <jats:styled-content style=\"fixed-case\">BCG<\/jats:styled-content> challenge. Furthermore, <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u2010\u03b3 expression increased in the lungs after <jats:styled-content style=\"fixed-case\">rR<\/jats:styled-content>v1737c pretreatment compared to that in the sham mice. Accordingly, lung cells from <jats:styled-content style=\"fixed-case\">rR<\/jats:styled-content>v1737c\u2010immunized mice stimulated with killed <jats:styled-content style=\"fixed-case\">BCG<\/jats:styled-content> produced higher levels of multiple cytokines, such as <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u2010\u03b3, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201010 and <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106. The results confirmed that the pathological features of <jats:styled-content style=\"fixed-case\">rR<\/jats:styled-content>v1737c promoted inflammation. Overall, our findings provide direct evidence of the pro\u2010inflammatory function of <jats:styled-content style=\"fixed-case\">rR<\/jats:styled-content>v1737c in a murine model of <jats:styled-content style=\"fixed-case\">BCG<\/jats:styled-content> infection, indicating that Rv1737c is a pathogenic antigen of <jats:italic>M.\u00a0tuberculosis<\/jats:italic> and may be key to the recurrence of latent infection.<\/jats:p>","DOI":"10.1111\/sji.12729","type":"journal-article","created":{"date-parts":[[2018,10,29]],"date-time":"2018-10-29T17:54:26Z","timestamp":1540835666000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["The DosR antigen Rv1737c from <i>Mycobacterium tuberculosis<\/i> confers inflammation regulation in tuberculosis 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