| First Author | Derbigny WA | Year | 2010 |
| Journal | J Immunol | Volume | 185 |
| Issue | 11 | Pages | 6689-97 |
| PubMed ID | 20974982 | Mgi Jnum | J:167371 |
| Mgi Id | MGI:4868141 | Doi | 10.4049/jimmunol.1001548 |
| Citation | Derbigny WA, et al. (2010) The Chlamydia muridarum-induced IFN-beta response is TLR3-dependent in murine oviduct epithelial cells. J Immunol 185(11):6689-97 |
| abstractText | Epithelial cells lining the murine genital tract act as sentinels for microbial infection, play a major role in the initiation of the early inflammatory response, and can secrete factors that modulate the adaptive immune response when infected with Chlamydia. C. muridarum-infected murine oviduct epithelial cells secrete the inflammatory cytokines IL-6 and GM-CSF in a TLR2-dependent manner. Further, C. muridarum infection induces IFN-beta synthesis in the oviduct epithelial cells in a TRIF-dependent manner. Because murine oviduct epithelial cells express TLR3 but not TLRs 4, 7, 8, or 9, we hypothesized that TLR3 or an unknown TRIF-dependent pattern recognition receptor was the critical receptor for IFN-beta production. To investigate the role of TLR3 in the Chlamydia-induced IFN-beta response in oviduct epithelial cells, we used small interfering RNA, dominant-negative TLR3 mutants, and TLR3-deficient oviduct epithelial cells to show that the IFN-beta secreted during C. muridarum infection requires a functional TLR3. Interestingly, we demonstrate that the TLR3 signaling pathway is not required for IFN-beta synthesis in C. muridarum-infected macrophages, suggesting that there are alternate and redundant pathways to Chlamydia-induced IFN-beta synthesis that seem to be dependent upon the cell type infected. Finally, because there is no obvious dsRNA molecule associated with Chlamydia infection, the requirement for TLR3 in Chlamydia-induced IFN-beta synthesis in infected oviduct epithelial cells implicates a novel ligand that binds to and signals through TLR3. |
