Research in the lab of Wilbert A. Derbigny, PhD is focused on characterizing the cellular immune responses of epithelial cells lining the lumen of the oviduct. This team of investigators is describing their contributions to the overall immune response to Chlamydia infections.
The central focus of the laboratory addresses the hypothesis that the IFN-β produced within the oviduct during genital tract Chlamydia infection is Toll-like receptor-3 (TLR3) dependent, and that the synthesis of this important regulatory cytokine has significant impact on the synthesis of a multitude of other inflammatory mediators that are required to clear Chlamydia infections. This hypothesis was proven correct in vitro by disrupting TLR3 expression in wild-type murine oviduct epithelial (OE) cells via si-RNA, and in experiments using OE cells derived from TLR3-deficient mice. The Derbigny Lab’s most recent in vivo findings show that TLR3-deficient mice exhibit higher bacterial loads, altered CD4+ T-cell recruitment, and more severe genital tract damage during intravaginal Chlamydia muridarum infection when compared to wild type mice. Collectively, our data implicate TLR3 as an important modulator of the immune response during genital tract Chlamydia infections in mice.