{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T00:40:40Z","timestamp":1791852040348,"version":"4.3.4"},"reference-count":89,"publisher":"eLife Sciences Publications, Ltd","license":[{"start":{"date-parts":[[2022,9,26]],"date-time":"2022-09-26T00:00:00Z","timestamp":1664150400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2022,9,26]],"date-time":"2022-09-26T00:00:00Z","timestamp":1664150400000},"content-version":"am","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2022,9,26]],"date-time":"2022-09-26T00:00:00Z","timestamp":1664150400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100000781","name":"European Research Council","doi-asserted-by":"publisher","award":["ERC-2018-ADG\/NCI-CAD"],"award-info":[{"award-number":["ERC-2018-ADG\/NCI-CAD"]}],"id":[{"id":"10.13039\/501100000781","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","award":["RTG 2157\/2"],"award-info":[{"award-number":["RTG 2157\/2"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["elifesciences.org"],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2022,9,13]]},"abstract":"<jats:p>\n                    <jats:italic>Chlamydia trachomatis (Ctr)<\/jats:italic>\n                    can persist over extended times within their host cell and thereby establish chronic infections. One of the major inducers of chlamydial persistence is interferon-gamma (IFN-\u03b3) released by immune cells as a mechanism of immune defence. IFN-\u03b3 activates the catabolic depletion of L-tryptophan (Trp) via indoleamine-2,3-dioxygenase (IDO), resulting in persistent\n                    <jats:italic>Ctr<\/jats:italic>\n                    . Here, we show that IFN-\u03b3 induces the downregulation of c-Myc, the key regulator of host cell metabolism, in a STAT1-dependent manner. Expression of c-Myc rescued\n                    <jats:italic>Ctr<\/jats:italic>\n                    from IFN-\u03b3-induced persistence in cell lines and human fallopian tube organoids. Trp concentrations control c-Myc levels most likely via the PI3K-GSK3\u03b2 axis. Unbiased metabolic analysis revealed that\n                    <jats:italic>Ctr<\/jats:italic>\n                    infection reprograms the host cell tricarboxylic acid (TCA) cycle to support pyrimidine biosynthesis. Addition of TCA cycle intermediates or pyrimidine\/purine nucleosides to infected cells rescued\n                    <jats:italic>Ctr<\/jats:italic>\n                    from IFN-\u03b3-induced persistence. Thus, our results challenge the longstanding hypothesis of Trp depletion through IDO as the major mechanism of IFN-\u03b3-induced metabolic immune defence and significantly extends the understanding of the role of IFN-\u03b3 as a broad modulator of host cell metabolism.\n                  <\/jats:p>","DOI":"10.7554\/elife.76721","type":"journal-article","created":{"date-parts":[[2022,9,13]],"date-time":"2022-09-13T07:15:26Z","timestamp":1663053326000},"update-policy":"https:\/\/doi.org\/10.7554\/elife.76721","source":"Crossref","is-referenced-by-count":28,"title":["c-Myc plays a key role in IFN-\u03b3-induced persistence of Chlamydia trachomatis"],"prefix":"10.7554","volume":"11","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1003-4410","authenticated-orcid":true,"given":"Nadine","family":"Vollmuth","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00fbnyb24","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology, Biocenter, University of 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