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Using the<jats:named-content content-type=\"genus-species\">Chlamydia muridarum<\/jats:named-content>genital infection model of mice, which replicates many features of human<jats:named-content content-type=\"genus-species\">C. trachomatis<\/jats:named-content>infection and avoids the characteristic low virulence of<jats:named-content content-type=\"genus-species\">C. trachomatis<\/jats:named-content>in the mouse, we previously demonstrated a significant role for antibody in immunity to chlamydial infection. We found that antibody alone was not protective. Instead, protection appeared to be conferred through an undefined antibody-cell interaction. Using gene knockout mice and<jats:italic>in vivo<\/jats:italic>cellular depletion methods, our data suggest that antibody-mediated protection is dependent on the activation of an effector cell population in genital tract tissues by CD4<jats:sup>+<\/jats:sup>T cells. Furthermore, the CD4<jats:sup>+<\/jats:sup>T cell-secreted cytokine gamma interferon (IFN-\u03b3) was found to be a key component of the protective antibody response. The protective function of IFN-\u03b3 was not related to the immunoglobulin class or to the magnitude of the<jats:named-content content-type=\"genus-species\">Chlamydia<\/jats:named-content>-specific antibody response or to recruitment of an effector cell population to genital tract tissue. Rather, IFN-\u03b3 appears to be necessary for activation of the effector cell population that functions in antibody-mediated chlamydial immunity. Our results confirm the central role of antibody in immunity to chlamydia reinfection and demonstrate a key function for IFN-\u03b3 in antibody-mediated protection.<\/jats:p>","DOI":"10.1128\/iai.00749-16","type":"journal-article","created":{"date-parts":[[2016,9,7]],"date-time":"2016-09-07T01:30:00Z","timestamp":1473211800000},"page":"3232-3242","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":55,"title":["Gamma Interferon Is Required for Optimal Antibody-Mediated Immunity against Genital Chlamydia Infection"],"prefix":"10.1128","volume":"84","author":[{"given":"Elizabeth K.","family":"Naglak","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sandra G.","family":"Morrison","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9747-9884","authenticated-orcid":false,"given":"Richard P.","family":"Morrison","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","volume-title":"Global Incidence and prevalence of selected curable sexually transmitted infections-2008","author":"World Health Organization","year":"2012","unstructured":"World Health Organization. 2012. 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