{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,4]],"date-time":"2026-09-04T14:15:07Z","timestamp":1788531307143,"version":"build-2803163510"},"reference-count":144,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,4]],"date-time":"2026-09-04T00:00:00Z","timestamp":1788480000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cell. Infect. Microbiol."],"abstract":"<jats:p>\n                    Tuberculosis is a chronic infectious disease caused by\n                    <jats:italic>Mycobacterium tuberculosis<\/jats:italic>\n                    (Mtb). As primary host cells targeted by Mtb, macrophages play central roles in both innate and adaptive immunity. Accumulating evidence indicates that macrophage polarization is a key determinant of tuberculosis pathogenesis. In response to diverse microenvironmental cues, macrophages adopt functionally distinct polarization states, ranging from pro-inflammatory, microbicidal programs (M1-like) to anti-inflammatory, tissue-reparative programs (M2-like). These states differentially shape tuberculosis progression. Defining the remodeling of these context-dependent macrophage states is therefore critical for understanding Mtb infection, granuloma formation, and disease outcomes, as well as for guiding the development of next-generation vaccines, immunotherapies, and host-directed interventions. This Review synthesizes the molecular mechanisms underlying macrophage polarization during Mtb infection, integrates the bidirectional regulatory networks between pathogen-derived and host-derived factors, and highlights their roles in immune evasion, granuloma biology, and emerging therapeutic strategies in tuberculosis.\n                  <\/jats:p>","DOI":"10.3389\/fcimb.2026.1913094","type":"journal-article","created":{"date-parts":[[2026,9,4]],"date-time":"2026-09-04T13:23:08Z","timestamp":1788528188000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Macrophage states and polarization during Mycobacterium tuberculosis infection: mechanisms, granuloma adaptation, and host-directed therapeutic opportunities"],"prefix":"10.3389","volume":"16","author":[{"given":"Minglong","family":"Xu","sequence":"first","affiliation":[{"name":"Department of General Practice, Affiliated Hospital of Zunyi Medical University","place":["Zunyi, Guizhou, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhangli","family":"Peng","sequence":"additional","affiliation":[{"name":"Department of General Practice, Affiliated Hospital of Zunyi Medical University","place":["Zunyi, Guizhou, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,9,4]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"9","DOI":"10.1016\/j.molcel.2010.09.014","article-title":"CRL4(Cdt2) regulates cell proliferation and histone gene expression by targeting PR-Set7\/Set8 for degradation","volume":"40","author":"Abbas","year":"2010","journal-title":"Mol. 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