{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,7,27]],"date-time":"2026-07-27T06:02:18Z","timestamp":1785132138780,"version":"3.55.0"},"posted":{"date-parts":[[2026,7,22]]},"group-title":"Immunology","reference-count":62,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2026,7,22]],"date-time":"2026-07-22T00:00:00Z","timestamp":1784678400000},"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":[[2026,7,22]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                <jats:p>\n                  Following an intravaginal inoculation with\n                  <jats:italic>Chlamydia trachomatis<\/jats:italic>\n                  , mice deficient in type I interferon receptor IFN\u03b1R1 (IFN\u03b1R1\n                  <jats:sup>-\/-<\/jats:sup>\n                  ) significantly increased the yield of live chlamydiae on days 3 &amp; 5 but reduced it to the level of wild-type mice by day 7, while mice deficient in type II interferon receptor IFN\u03b3R1 (IFN\u03b3R1\n                  <jats:sup>-\/-<\/jats:sup>\n                  ) significantly increased the chlamydial yield by day 5 and the increase persisted throughout the remainder of the infection course. These observations reveal a temporal division of labor between type I &amp; II interferons in regulating\n                  <jats:italic>C. trachomatis<\/jats:italic>\n                  infection in the female genital tract. Interestingly, mice deficient in both IFN\u03b1R1 &amp; IFN\u03b3R1 exhibited higher mortality and shed more chlamydial organisms than IFN\u03b3R1\n                  <jats:sup>-\/-<\/jats:sup>\n                  mice by week 6, suggesting that IFN\u03b1R1 remains critical for inhibiting\n                  <jats:italic>C. trachomatis<\/jats:italic>\n                  at late stages. An anti-IFN\u03b1R1 antibody blockade significantly increased chlamydial yields in IFN\u03b3R1\n                  <jats:sup>-\/-<\/jats:sup>\n                  mice, suggesting that the anti-chlamydial activities of type I &amp; II interferon systems are both distinct and overlapping throughout the infection course. Furthermore, the anti-chlamydial activity of type I interferon signaling is localized to the lower vagina, while that of type II interferon signaling is localized to the upper vagina. Thus, we have demonstrated that type I &amp; II interferons function complementarily and synergistically in time and space to control\n                  <jats:italic>C. trachomatis<\/jats:italic>\n                  infection, laying the foundation for further elucidating the mechanisms of IFN regulation of chlamydial infection and for developing interventional and preventive strategies against\n                  <jats:italic>C. trachomatis<\/jats:italic>\n                  in the female genital tract.\n                <\/jats:p>\n                <jats:sec>\n                  <jats:title>Importance<\/jats:title>\n                  <jats:p>Lack of information on the precise roles of type I and type II interferons during chlamydial infection has hindered the development of interferon-based strategies to prevent chlamydial infection and pathogenicity. The current study has revealed a temporal division of labor between type I &amp; type II interferons in regulating chlamydial infection in the female genital tract, with type I acting earlier than type II during the innate phase. Nevertheless, type I remains critical for cooperating with type II to suppress chlamydia 6 weeks after infection. Finally, type I interferons seem to mainly target chlamydial infection in the lower vagina, while type II interferons target the infection in the upper vagina. These new findings on the distinct and overlapping roles of type I and type II interferons in regulating chlamydial infection may guide the development of interferon-based precision strategies to reduce chlamydial infection and pathogenicity in the female genital tract.<\/jats:p>\n                <\/jats:sec>","DOI":"10.64898\/2026.07.17.739123","type":"posted-content","created":{"date-parts":[[2026,7,27]],"date-time":"2026-07-27T05:46:47Z","timestamp":1785131207000},"source":"Crossref","is-referenced-by-count":0,"title":["Regulation of\n                  <i>Chlamydia trachomatis<\/i>\n                  infection in the female genital tract by type I and type II interferons"],"prefix":"10.64898","author":[{"given":"Rongze","family":"He","sequence":"first","affiliation":[{"name":"Department of Microbiology, Immunology and Molecular Genetics, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, Texas 78229, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yi","family":"Wu","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Immunology and Molecular Genetics, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, Texas 78229, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ahmed","family":"Abdelsalam","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Immunology and Molecular Genetics, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, Texas 78229, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yihui","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Biomedical Engineering, Pratt School of Engineering, Duke University, Durham, NC 27708, USA (yihui.wang@duke.edu)"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4903-926X","authenticated-orcid":false,"given":"Huizhou","family":"Fan","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Rutgers Medical School, 675 Hoes Lane, Room 400, Piscataway, NJ 08854, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7053-5009","authenticated-orcid":false,"given":"Guangming","family":"Zhong","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Immunology and Molecular Genetics, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, Texas 78229, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"54368","reference":[{"key":"2026072622270781000_2026.07.17.739123v1.1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra1411426"},{"key":"2026072622270781000_2026.07.17.739123v1.2","doi-asserted-by":"publisher","DOI":"10.1097\/AOG.0b013e3182519326"},{"key":"2026072622270781000_2026.07.17.739123v1.3","unstructured":"Janeway CA Jr TP, Walport M , et al. 2001. 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