{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T02:18:32Z","timestamp":1789525112318,"version":"build-2803163510"},"posted":{"date-parts":[[2025,12,9]]},"group-title":"Immunology","reference-count":102,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2025,12,9]],"date-time":"2025-12-09T00:00:00Z","timestamp":1765238400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.biorxiv.org\/about\/FAQ#license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,6,3]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                <jats:p>\n                  CD8\n                  <jats:sup>+<\/jats:sup>\n                  T cells are elicited during tuberculosis yet how susceptible lung environments shape their maintenance and behavior is unclear. We examined pulmonary T cell responses to\n                  <jats:italic>Mycobacterium tuberculosis<\/jats:italic>\n                  in resistant control and\n                  <jats:italic>\n                    Sp140\n                    <jats:sup>-\/-<\/jats:sup>\n                  <\/jats:italic>\n                  mice, a model of type I interferon (IFN-I)-driven susceptibility. Resistant mice generated diverse CD8\n                  <jats:sup>+<\/jats:sup>\n                  effector- and memory-like subsets producing TNF and IFN\u03b3, whereas\n                  <jats:italic>\n                    Sp140\n                    <jats:sup>-\/-<\/jats:sup>\n                  <\/jats:italic>\n                  mice showed a broad loss of pulmonary CD8\n                  <jats:sup>+<\/jats:sup>\n                  T cells. Single-cell RNA sequencing revealed altered states in CD8\n                  <jats:sup>+<\/jats:sup>\n                  T cells from susceptible mice with exhaustion and IFN-I transcriptional programs. IFNAR blockade rescued CD8\n                  <jats:sup>+<\/jats:sup>\n                  T cell numbers, diversity, cytokine production, reduced bacterial burden and lung pathology, with comparable benefits also valid for CD4\n                  <jats:sup>+<\/jats:sup>\n                  T cells. Intravital microscopy of infected lungs further showed that T cell dynamics and motility within lesions were restricted under exuberant IFN-I signaling but fully restored by IFNAR blockade. Thus, IFN-I-driven tissue pathology restricts T cell accumulation and motility during tuberculosis.\n                <\/jats:p>\n                <jats:sec>\n                  <jats:title>Teaser<\/jats:title>\n                  <jats:p>In tuberculosis, excessive type I interferon signaling reshapes the lung environment, limiting T cell accumulation and motility within infected lesions.<\/jats:p>\n                <\/jats:sec>","DOI":"10.64898\/2025.12.05.692491","type":"posted-content","created":{"date-parts":[[2025,12,9]],"date-time":"2025-12-09T20:15:27Z","timestamp":1765311327000},"source":"Crossref","is-referenced-by-count":4,"title":["Type I interferon\u2013driven lung pathology restricts T cell accumulation and motility during tuberculosis"],"prefix":"10.64898","author":[{"given":"Maxime","family":"Caouaille","sequence":"first","affiliation":[{"name":"Univ Toulouse, CNRS, IPBS, Toulouse, 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