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The immune response elicited by natural infection fails to protect against reinfection and can contribute to tissue inflammation and damage. CD4+ T cells are key mediators of protection against C. trachomatis. However, these same cells, together with neutrophils, also contribute to tissue pathology. The identity and effector functions of the CD4+ T cells that contribute to protection, pathology, or both remain poorly defined. Notably, C. trachomatis pathology is serovar specific. Infection with serovar D induces severe tissue inflammation in the female upper genital tract, whereas infection with serovar L2 does not. Using a murine model of genital infection, we found that infection with serovar D selectively drives the polarization of na\u00efve CD4+ T cells into inflammatory Th17 cells through the induction of Th17-polarizing cytokines, such as IL-1\u03b2, IL-6, and IL-23, compared with serovar L2 infection. Single-cell RNA sequencing of CD4+ T cells from the uteri of serovar D\u2013infected mice revealed a Th17-skewed response with transcriptional features of an inflammatory phenotype, including upregulation of Bhlhe40 and Il1r1. Th17 cells have been reported to contribute to pathology through secretion of pro-inflammatory cytokines that recruit neutrophils and promote tissue damage. Together, these findings demonstrate that serovar D promotes pro-inflammatory CD4+ T-cell responses that could contribute to immunopathology in C. trachomatis infection, in contrast to the response elicited by serovar L2. They also underscore the importance of developing a vaccine that elicits protective immunity while minimizing harmful inflammatory responses.<\/jats:p>","DOI":"10.1093\/jimmun\/vkag177","type":"journal-article","created":{"date-parts":[[2026,7,7]],"date-time":"2026-07-07T20:53:43Z","timestamp":1783457623000},"source":"Crossref","is-referenced-by-count":0,"title":["Inflammatory genital strain of\n                    <i>Chlamydia trachomatis<\/i>\n                    elicits a Th17 immune response"],"prefix":"10.1093","volume":"215","author":[{"given":"Andrea","family":"Lebron Figueroa","sequence":"first","affiliation":[{"name":"Department of Microbiology, Harvard Medical School , Boston, MA,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ian","family":"Magill","sequence":"additional","affiliation":[{"name":"Department of Immunology, Harvard Medical School , Boston, MA,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David","family":"Zemmour","sequence":"additional","affiliation":[{"name":"Committee on Immunology, University of Chicago , Chicago, IL,","place":["United States"]},{"name":"Department of Pathology, University of Chicago , Chicago, IL,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4465-712X","authenticated-orcid":false,"given":"Michael N","family":"Starnbach","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Harvard Medical School , Boston, MA,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2026,7,7]]},"reference":[{"key":"2026090710451391100_vkag177-B1","author":"Centers for Disease Control and Prevention","year":"2024"},{"key":"2026090710451391100_vkag177-B2","first-page":"834","article-title":"Prevalence of Chlamydia trachomatis 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