We have identified a CD8+CXCR5+ T cell that prevents the development of oviduct dilation following C. muridarum genital infection. Phenotypic studies show that CD8+CXCR5+ cells express markers of T regulatory cells (FoxP3, CD25, and GITR) but do not express a necessary component of cytotoxic cells (perforin). mice have significantly lower numbers of CD8+ cells and lack the CD8+CXCR5+ population while the total number of CD4+ cells is equivalent between mouse strains. The transfer of CD8+ splenocytes from WT mice reduces the oviduct dilation seen in mice following C. muridarum infection. Future studies will investigate the mechanism by which this cell type regulates genital tract pathology. 1. Introduction Pelvic inflammatory disease (PID) is defined as inflammation of the uterus and/or fallopian tubes and is induced by a number of organisms following sexual transmission. Chlamydia trachomatis is the most common reportable sexually transmitted infection (STI) and is responsible for >1 million cases in the US and approximately 92 million cases worldwide each year [1, 2]. Genital infection can lead to immune-mediated damage of the female reproductive organs and serious reproductive disability, including PID that can result in chronic pelvic pain, ectopic pregnancy, and infertility [3]. The risk of developing infertility increases by 40%–70% following reinfection [4]. The reinfection rate is approximately 13% and occurs within 6 months [5]. Delivery of treatments designed to reduce the local inflammation and prevent fibrotic disease to infected individuals may be a viable approach for further reducing PID and the costs associated with its treatment. Regulatory T cells (Tregs) are comprised of multiple subsets of T cells that suppress other T cells from engaging in detrimental immune responses [6]. Tregs are broadly categorized as natural or inducible. Natural Tregs induce tolerance, delete autoreactive T cells, and dampen inflammation during an autoimmune reaction [7–13]. Inducible Tregs arise during infections in response to the infectious process to restore the homeostatic environment. In some cases, Tregs can be actively induced by the pathogen and promote pathogen survival by preventing elimination [14]. Tregs have also been shown to protect mucosal surfaces of the intestine from inflammation [15]. The linage can be phenotypically identified by the Foxp3 transcription factor [16]. The most widely studied subset is phenotypically defined as CD4+CD25+FoxP3+. This subset has been shown to indirectly prolong microbial growth by interfering with the priming
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