{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,19]],"date-time":"2026-08-19T18:32:49Z","timestamp":1787164369870,"version":"build-2736575974"},"reference-count":49,"publisher":"American Society for Microbiology","issue":"4","license":[{"start":{"date-parts":[[2017,4,1]],"date-time":"2017-04-01T00:00:00Z","timestamp":1491004800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/100000060","name":"HHS | NIH | National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["R01AI093692"],"award-info":[{"award-number":["R01AI093692"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100006108","name":"HHS | NIH | National Center for Advancing Translational Sciences","doi-asserted-by":"publisher","award":["UL1TR001417"],"award-info":[{"award-number":["UL1TR001417"]}],"id":[{"id":"10.13039\/100006108","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Clin Vaccine Immunol"],"published-print":{"date-parts":[[2017,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    <jats:named-content content-type=\"genus-species\">Chlamydia trachomatis<\/jats:named-content>\n                    infection is the most prevalent bacterial sexually transmitted infection and can cause significant reproductive morbidity in women. There is insufficient knowledge of\n                    <jats:named-content content-type=\"genus-species\">C. trachomatis<\/jats:named-content>\n                    -specific immune responses in humans, which could be important in guiding vaccine development efforts. In contrast, murine models have clearly demonstrated the essential role of T helper type 1 (Th1) cells, especially interferon gamma (IFN-\u03b3)-producing CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells, in protective immunity to chlamydia. To determine the frequency and magnitude of Th1 cytokine responses elicited to\n                    <jats:named-content content-type=\"genus-species\">C. trachomatis<\/jats:named-content>\n                    infection in humans, we stimulated peripheral blood mononuclear cells from 90 chlamydia-infected women with\n                    <jats:named-content content-type=\"genus-species\">C. trachomatis<\/jats:named-content>\n                    elementary bodies, Pgp3, and major outer membrane protein and measured IFN-\u03b3-, tumor necrosis factor alpha (TNF-\u03b1)-, and interleukin-2 (IL-2)-producing CD4\n                    <jats:sup>+<\/jats:sup>\n                    and CD8\n                    <jats:sup>+<\/jats:sup>\n                    T-cell responses using intracellular cytokine staining. The majority of chlamydia-infected women elicited CD4\n                    <jats:sup>+<\/jats:sup>\n                    TNF-\u03b1 responses, with frequency and magnitude varying significantly depending on the\n                    <jats:named-content content-type=\"genus-species\">C. trachomatis<\/jats:named-content>\n                    antigen used. CD4\n                    <jats:sup>+<\/jats:sup>\n                    IFN-\u03b3 and IL-2 responses occurred infrequently, as did production of any of the three cytokines by CD8\n                    <jats:sup>+<\/jats:sup>\n                    T cells. About one-third of TNF-\u03b1-producing CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells coproduced IFN-\u03b3 or IL-2. In summary, the predominant Th1 cytokine response elicited to\n                    <jats:named-content content-type=\"genus-species\">C. trachomatis<\/jats:named-content>\n                    infection in women was a CD4\n                    <jats:sup>+<\/jats:sup>\n                    TNF-\u03b1 response, not CD4\n                    <jats:sup>+<\/jats:sup>\n                    IFN-\u03b3, and a subset of the CD4\n                    <jats:sup>+<\/jats:sup>\n                    TNF-\u03b1-positive cells produced a second Th1 cytokine.\n                  <\/jats:p>","DOI":"10.1128\/cvi.00010-17","type":"journal-article","created":{"date-parts":[[2017,1,18]],"date-time":"2017-01-18T21:11:40Z","timestamp":1484773900000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":24,"title":["The Predominant CD4\n                    <sup>+<\/sup>\n                    Th1 Cytokine Elicited to Chlamydia trachomatis Infection in Women Is Tumor Necrosis Factor Alpha and Not Interferon Gamma"],"prefix":"10.1128","volume":"24","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4063-2566","authenticated-orcid":false,"given":"Stephen J.","family":"Jordan","sequence":"first","affiliation":[{"name":"Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kanupriya","family":"Gupta","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brian M. O.","family":"Ogendi","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rakesh K.","family":"Bakshi","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richa","family":"Kapil","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christen G.","family":"Press","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steffanie","family":"Sabbaj","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeannette Y.","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William M.","family":"Geisler","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","volume-title":"WHO guidelines for the treatment of Chlamydia trachomatis","author":"World Health Organization","year":"2016","unstructured":"World Health Organization. 2016. 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