Innate IFN-{gamma} Is Essential for Systemic Chlamydia muridarum Control in Mice, While CD4 T Cell-Dependent IFN-{gamma} Production Is Highly Redundant in the Female Reproductive Tract [Microbial Immunity and Vaccines]

In this study, we dissected the requirements of IFN- produced by innate immune cells and CD4 T cells for resolution of Chlamydia muridarum female reproductive tract (FRT) infection. After C. muridarum intravaginal infection, IFN--deficient and T cell-deficient mice exhibited opposite phenotypes for survival and bacterial shedding at the FRT mucosa, demonstrating the distinct requirements for IFN- and CD4 T cells in host defense against Chlamydia. In Rag1-deficient mice, IFN- produced by innate lymphocytes (ILCs) accounted for early bacterial control and prolonged survival in the absence of adaptive immunity. Although type I ILCs are potent IFN- producers, we found that mature NK cells and ILC1s were not the sole sources of innate IFN- in response to Chlamydia. By conducting T cell adoptive transfer, we showed definitively that IFN--deficient CD4 T cells were sufficient for effective bacterial killing in the FRT during the first 21 days of infection and reduced bacterial burden more than 1,000-fold, although mice receiving IFN--deficient CD4 T cells failed to completely eradicate the bacteria from the FRT like their counterparts receiving wild-type (WT) CD4 T cells. Together, our results revealed that innate IFN- is essential for preventing systemic Chlamydia dissemination, whereas IFN- produced by CD4 T cells is largely redundant at the FRT mucosa.
Source: Infection and Immunity - Category: Infectious Diseases Authors: Tags: Microbial Immunity and Vaccines Source Type: research