Non-canonical IRF3 functions in limiting pulmonary inflammation

Title : Non-canonical IRF3 functions in limiting pulmonary inflammation

Abstract:

The interferon (IFN) system is a cornerstone of host defense against viral infection, coordinating antiviral immunity while simultaneously shaping inflammatory responses. Although inflammation is required for effective viral control, excessive cytokine production underlies much of the tissue injury, respiratory failure, and mortality observed in severe viral diseases. Our work seeks to define regulatory nodes within the IFN signaling network that uncouple antiviral protection from pathological inflammation. Using primary human and murine cells together with clinically relevant mouse models of respiratory viral infection, we have identified host-intrinsic pathways that selectively restrain cytokine amplification without impairing antiviral immunity. These findings reveal tractable mechanisms that may be therapeutically leveraged to limit cytokine-driven immunopathology and improve outcomes in acute respiratory viral infections.

Biography:

Saurabh Chattopadhyay, Ph.D., is an Associate Professor in the Department of Microbiology, Immunology, and Molecular Genetics at the University of Kentucky College of Medicine. His research investigates how viral pathogens interface with innate immune signaling pathways, with a particular focus on interferon-regulated mechanisms that shape antiviral defense and inflammatory responses. His laboratory has been funded by the National Institutes of Health, the Ohio Department of Health, the Centers for Disease Control and Prevention, and the American Heart Association. Dr. Chattopadhyay earned his doctoral degree in Biotechnology from the Indian Institute of Technology Delhi and completed postdoctoral training in Virology at the Cleveland Clinic. Before joining the University of Kentucky, he was a faculty member at the University of Toledo College of Medicine.