{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T03:03:33Z","timestamp":1787022213616,"version":"build-2736575974"},"update-to":[{"DOI":"10.1371\/journal.ppat.1013208","type":"new_version","label":"New version","source":"publisher","updated":{"date-parts":[[2025,6,25]],"date-time":"2025-06-25T00:00:00Z","timestamp":1750809600000}}],"reference-count":98,"publisher":"Public Library of Science (PLoS)","issue":"6","license":[{"start":{"date-parts":[[2025,6,9]],"date-time":"2025-06-09T00:00:00Z","timestamp":1749427200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["R01AI103760"],"award-info":[{"award-number":["R01AI103760"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["2T32HL007062"],"award-info":[{"award-number":["2T32HL007062"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["R01AI173780"],"award-info":[{"award-number":["R01AI173780"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["K08AI150425"],"award-info":[{"award-number":["K08AI150425"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["www.plospathogens.org"],"crossmark-restriction":false},"short-container-title":["PLoS Pathog"],"abstract":"<jats:p>\n                    Although lung myeloid cells provide an intracellular niche for\n                    <jats:italic>Mycobacterium tuberculosis<\/jats:italic>\n                    (\n                    <jats:italic>Mtb<\/jats:italic>\n                    ), CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells limit\n                    <jats:italic>Mtb<\/jats:italic>\n                    growth in these cells to protect the host. The CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cell activities including interferon-\u03b3 (IFN-\u03b3) production that account for this protection are poorly understood. Using intravenous antibody labeling and lineage-tracing reporter mice, we show that monocyte-derived macrophages (MDMs), rather than phenotypically similar monocytes or dendritic cells, are preferentially infected with\n                    <jats:italic>Mtb<\/jats:italic>\n                    in murine lungs. MDMs were recruited to the lungs by\n                    <jats:italic>Mtb-<\/jats:italic>\n                    specific CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells via IFN-\u03b3, which promoted the extravasation of monocyte precursors from the blood. It was possible that CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells recruited infectable MDMs because these cells are uniquely poised to receive cognate MHCII-mediated help to control intracellular bacteria. Mice with MHCII deficiency in monocyte-derived cells had normal\n                    <jats:italic>Mtb<\/jats:italic>\n                    -specific CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cell activation, expansion and differentiation but the CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells were unable to attenuate\n                    <jats:italic>Mtb<\/jats:italic>\n                    growth. Using single cell RNA sequencing, we showed that MDMs receiving cognate MHCII-mediated help from CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells upregulated glycolytic genes associated with\n                    <jats:italic>Mtb<\/jats:italic>\n                    control. Overall, the results indicate that CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells recruit infectable MDMs to the lungs and then trigger glycolysis-dependent bacterial control in the MDMs by engaging their MHCII-bound\n                    <jats:italic>Mtb<\/jats:italic>\n                    peptides. Moreover, the results suggest that cognate MHCII-mediated help to promote MDM glycolysis is an essential, IFN-\u03b3-independent effector function of\n                    <jats:italic>Mtb<\/jats:italic>\n                    -specific CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells.\n                  <\/jats:p>","DOI":"10.1371\/journal.ppat.1013208","type":"journal-article","created":{"date-parts":[[2025,6,9]],"date-time":"2025-06-09T13:55:07Z","timestamp":1749477307000},"page":"e1013208","update-policy":"https:\/\/doi.org\/10.1371\/journal.ppat.corrections_policy","source":"Crossref","is-referenced-by-count":11,"title":["Antigen-specific CD4+ T cells promote monocyte recruitment and differentiation into glycolytic lung macrophages to control Mycobacterium tuberculosis"],"prefix":"10.1371","volume":"21","author":[{"given":"Samuel H.","family":"Becker","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christine E.","family":"Ronayne","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7360-6546","authenticated-orcid":true,"given":"Tyler D.","family":"Bold","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8009-7655","authenticated-orcid":true,"given":"Marc K.","family":"Jenkins","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"340","published-online":{"date-parts":[[2025,6,9]]},"reference":[{"issue":"1","key":"ppat.1013208.ref001","doi-asserted-by":"crossref","first-page":"16076","DOI":"10.1038\/nrdp.2016.76","article-title":"Tuberculosis","volume":"2","author":"M Pai","year":"2016","journal-title":"Nature Reviews Disease 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