MI2025 – Chun Howe Ng

Title:
Deciphering the role of the Type III Interferon (Interferon-λ) in the Chlamydia trachomatis infection-associated fibrosis

Abstract:
Chlamydia trachomatis is the most common bacterial sexually transmitted infection globally, posing significant risks for reproductive health, including pelvic inflammatory disease, infertility, and ectopic pregnancy. As an obligate intracellular pathogen, C. trachomatis primarily targets vaginal epithelial cells, where it establishes persistent infections while evading immune surveillance. Type III interferons (IFN-λ) are key cytokines in mucosal immunity, offering localized protection with minimal systemic inflammation due to the restricted expression of their receptor complex (IFNLR1/IL-10R2) on epithelial tissues. This study investigates the interaction between type III IFNs and C. trachomatis infection in epithelial cells. Our study reveals that C. trachomatis interferes with the expression of signaling proteins, suggesting a potential immune evasion mechanism employed by C. trachomatis to dampen type III IFN signaling. Understanding this regulatory dynamic provides novel insight into host-pathogen interactions and highlights the potential of targeting the IFN-λ pathway to develop therapeutic interventions that enhance mucosal immunity while limiting inflammation during C. trachomatis infection.

Biography:
I am a PhD student at the Department of Medical Microbiology, Faculty of Medicine, Universiti Malaya, Kuala Lumpur, Malaysia. My research mainly focuses on the role of type III interferons (IFNs) in Chlamydia trachomatis infection and their potential as therapeutic targets. My work explores how IFN signaling pathways, particularly the IFNλ1-IFNLR1 axis, influence cellular responses during infection.