Inflammation induces lymphoid aggregates suggestive of lymphoid neogenesis in both murine and human genital tracts after infection with Chlamydia. Lymphoid neogenesis refers to the accumulation of mononuclear cells which organize into distinct regions forming structures which resemble secondary lymphoid tissue. The regulation of lymphoid neogenesis has been implicated in tissue dysfunction. In particular, CXCL13, a homeostatic chemokine necessary in formation of secondary lymphoid tissue in utero, was expressed in both in vitro and in vivo models. In the in vitro model, we used organ cultures of human fallopian tissue (HFT) which was infected with C. trachomatis serovar E. We noted a 30-fold increase in mRNA for CXCL13 and found expression of CXCL13 in endothelium and stromal cells. Using the murine model for in vivo studies, we found CXCL13 induced in oviducts of Chlamydia-infected mice. An alteration in the level or duration of bacterial burden in the genital tract was not observed in treated mice. Surprisingly, anti-CXCL13 treatment significantly extended oviduct diameters, a measure of inflammation, 3 weeks after resolution of genital infection (7.5 + 1.2 goat IgG versus 43.7 + 8.7 anti-CXCL13; n = 3–4/grp, = 0.038, n = 4, t-test). Lastly, ectopic lymphoid tissue in known cases of human salpingitis was found to express CXCL13 and other characteristics of lymphoid neogenesis. This data indicates that CXCL13 plays a role in immune-mediated fallopian tube dysfunction. (NIH-AI-26328, AI-148146 & Iris-Cantor-UCLA fund).