Asset Details
Do you wish to reserve the book?
IFN-I exacerbates the inflammatory response of epithelial cells to Chlamydia trachomatis infection by enhancing TLR3 expression
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
IFN-I exacerbates the inflammatory response of epithelial cells to Chlamydia trachomatis infection by enhancing TLR3 expression
Do you wish to request the book?
IFN-I exacerbates the inflammatory response of epithelial cells to Chlamydia trachomatis infection by enhancing TLR3 expression
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
IFN-I exacerbates the inflammatory response of epithelial cells to Chlamydia trachomatis infection by enhancing TLR3 expression
2026
Overview
The effect of the production of IFN-I upon infection by Chlamydia trachomatis is not well understood. We showed that IFN-I exacerbated Chlamydia -induced inflammation in epithelial cells. This synergy was mediated by the IFN-induced upregulation of Toll-like receptor 3 (TLR3) expression, which facilitated sensing of Chlamydia and amplified the inflammatory response. We identified the signaling cascades involved upstream and downstream of TLR3 signaling. By exacerbating the pro-inflammatory response of epithelial cells, IFN-I might contribute to the hyperinflammation experienced by some individuals. The signaling pathways we uncovered can serve as a starting point for novel therapeutic strategies to alleviate tissue damage upon Chlamydia infection.
Publisher
ASM,American Society for Microbiology,American Society for Microbiology (ASM)
Subject
/ Chlamydia Infections - immunology
/ Chlamydia Infections - microbiology
/ Chlamydia trachomatis - immunology
/ Clinical Microbiology and Infectious Diseases
/ Epithelial Cells - immunology
/ Epithelial Cells - microbiology
/ Female
/ Humans
/ Inflammatory Mediators (Cytokines, Chemokines)
/ Interferon Type I - immunology
/ Interferon Type I - metabolism
/ Microbial Pathogenesis and Immunology
/ Pathogenesis and Host Response
/ Role in Host-Pathogen Interactions
/ synergy
/ Toll-Like Receptor 3 - genetics
