Myeloid cells are highly adaptable sentinel cells that continuously sense environmental cues and orchestrate immune responses to infection and tissue damage. Their remarkable phenotypic plasticity allows them to adopt distinct functional states that can either promote host protection or drive disease.

In this project, we investigate how environmental signals reprogram myeloid cells into disease-associated states during infection and autoimmunity. We focus on the molecular pathways by which myeloid cells integrate inflammatory signals and translate them into functional phenotypes that shape downstream immune responses.

Using integrated multi-omic profiling, advanced imaging approaches, and functional antigen-presentation assays, we identify signals that drive pathogenic myeloid cell phenotypes and define their consequences for immune regulation and disease progression.