{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,27]],"date-time":"2026-06-27T06:11:09Z","timestamp":1782540669693,"version":"3.54.5"},"reference-count":61,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,3,4]],"date-time":"2026-03-04T00:00:00Z","timestamp":1772582400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100004359","name":"Vetenskapsr\u00e5det","doi-asserted-by":"publisher","award":["23-02296"],"award-info":[{"award-number":["23-02296"]}],"id":[{"id":"10.13039\/501100004359","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003793","name":"Hj\u00e4rt-Lungfonden","doi-asserted-by":"publisher","award":["24-26\/20230249"],"award-info":[{"award-number":["24-26\/20230249"]}],"id":[{"id":"10.13039\/501100003793","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>Type I interferon (IFN-I) responses correlate with the severity of Tuberculosis. ISG15, a ubiquitin-like protein, regulates immune responses intracellularly by protein posttranslational modification (ISGylation) or extracellularly, in a cytokine-like manner. The ubiquitin specific protease USP18 deconjugates ISG15 from target proteins and is a major negative regulator of IFN-I signaling.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Here we show that\n                      <jats:italic>M. tuberculosis<\/jats:italic>\n                      infection induces ISGylation associated transcripts in murine bone marrow-derived macrophages (BMM). The expression of these transcripts was dependent on IFN-I signaling and was further enhanced by supplementation of IFN-\u03b2, but not with IFN-\u03b3 or IL-1\u03b2. While stimulation with IFN-\u03b2 impaired the intracellular control of\n                      <jats:italic>M. tuberculosis<\/jats:italic>\n                      in BMM, the bacterial growth was not altered by addition of extracellular ISG15. Treatment with two USP18 inhibitors, increased the ISGylation in uninfected and\n                      <jats:italic>M. tuberculosis<\/jats:italic>\n                      -infected BMM.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      The inhibition of USP18 enhanced both IFN-I responses and antimicrobial responses in BMM and increased NF-\u03baB-activation and IL-1\u03b2 expression. Moreover, the USP18 inhibitors improved the intracellular macrophage control of\n                      <jats:italic>M. tuberculosis<\/jats:italic>\n                      in an IFN-I independent manner. Instead, the addition of IFN-\u03b2 to the BMM cultures at least partially reversed the bacterial control conferred by the USP18 inhibition.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Discussion<\/jats:title>\n                    <jats:p>Our results suggest that the pharmacological inhibition of USP18 can be further explored as a therapeutic tool in the control of tuberculosis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fimmu.2026.1739628","type":"journal-article","created":{"date-parts":[[2026,3,4]],"date-time":"2026-03-04T07:00:24Z","timestamp":1772607624000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["Pharmacological inhibition of USP18 improves antibacterial responses and the intracellular control of Mycobacterium tuberculosis in 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