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Herein, we report that MafB in macrophages is a regulator of the pro-inflammatory cytokines, TNF-\u03b1 and IL-12p40, which are crucial for host defense against <jats:italic><jats:italic>M. tuberculosis<\/jats:italic><\/jats:italic> infection. Cell-based luciferase assays showed that MafB inhibited TNF-\u03b1 and IL-12p40 transcriptional activity in a dose-dependent manner. At the molecular level, MafB interacted with IFN regulatory factor (IRF)-5 and PU.1 and inhibited IRF-5- and PU.1-mediated transactivation, via the basic-leucine zipper domain. Analysis using gene-deficient macrophages demonstrated that the suppressed pro-inflammatory cytokine production during <jats:italic><jats:italic>M. tuberculosis<\/jats:italic><\/jats:italic> infection depends on MafB expression. Finally, <jats:italic><jats:italic>in vivo<\/jats:italic><\/jats:italic> studies indicated that <jats:italic><jats:italic>M. tuberculosis<\/jats:italic><\/jats:italic>-mediated increase of MafB expression was responsible for the exacerbation of <jats:italic><jats:italic>M. tuberculosis<\/jats:italic><\/jats:italic> infection. Thus, our results provide a functional view of MafB as a cytokine regulator as well as novel insights into host factors involved in TB susceptibility.<\/jats:p>","DOI":"10.1371\/journal.ppat.1013476","type":"journal-article","created":{"date-parts":[[2025,9,4]],"date-time":"2025-09-04T17:59:08Z","timestamp":1757008748000},"page":"e1013476","update-policy":"https:\/\/doi.org\/10.1371\/journal.ppat.corrections_policy","source":"Crossref","is-referenced-by-count":1,"title":["Mycobacterium tuberculosis impairs protective cytokine production via transcription factor MafB 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