Fig 4. C. trachomatis-specific CD4⁺ T cells displayed T_H1 and T_H17 effector function, but control of ivag C. trachomatis challenge is mainly mediated by T_H1 immunity.

At 60 dpi, mice were ivag challenged with 10⁶ IFU of C. trachomatis serovar D. At 5 dpc, animals were euthanized, DLN excised and processed into single-cell suspensions, and cells incubated with inactivated Chlamydia EB or media alone. (A) Representative contour plots from the intracellular cytokine staining (ICS) assay used to quantify secretion of IFN-γ, TNF, IL-17, and IL-4 by CD4⁺ and CD8⁺ T cells that responded to stimulation with Chlamydia EB; (quadrant numbers indicate percentages of cytokine-producing cells). (B) Percentages of cytokine-producing CD4⁺ and CD8⁺ T cells; (n = 13) (bars indicate medians). (C) Using additional Balb/cJ mice at 60 dpi, 10⁶ IFU of C. trachomatis serovar D was ivag administered to untreated controls or mice treated with antibodies blocking IFN-γ, IL-17, or IFN-γ and IL-17 signaling concomitant with challenge. At various days after challenge, CVL specimens were collected to measure Chlamydia DNA levels via RT-qPCR. AUC analysis for bacterial clearance revealed that Chlamydia challenge was primarily controlled by T_H1 immunity; (n = 5 per group) (values are means ±SD) (results representative of 2 independently performed studies) (ND, non-detectable).