Reducing pro-inflammatory cytokine signaling during priming increased the protective capacity of CD8+ T cells following transcervical Chlamydia infection. (A–D) CD90.1 mice were i.v. infected with C. trachomatis and treated with isotype control or antibodies to deplete cytokines on day 4 p.i. On day 28 p.i., CD8+ T cells were purified from pooled secondary lymphoid organs, CFSE-labeled, and transferred into naïve CD90.2 mice. The recipient mice and control mice that did not receive any T cells (no transfer) were transcervically infected with C. trachomatis. (A) The number of donor cells, (B) CFSEdim % among donor cells, (C) CD62L MFI of donor cells, and (D) Chlamydia burden in the uterus on day 6 p.i. are shown. (E) Mice were transcervically infected with C. trachomatis, and treated with isotype control or antibodies to deplete cytokines on day 4 p.i. On day 28 p.i., these mice and naïve mice (primary) were challenged transcervically with VacCrpA. Viral burden in the uterus on day 6 p.i is shown. Data are representative of at least two experiments, each with 6–7 mice per group.