Dr. Borghesi's research focuses on HSCs, the sole source of blood forming cells throughout life. It has long been known that infection triggers dramatic and rapid changes in hematopoietic output but the mechanisms remain murky. TLR4 is a dominant innate immune sensor for LPS and hence a model receptor for how the hematopoietic system adapts to pathogen exposure. Her laboratory is studying the mechanisms that enable stem cells to directly sense infection, and functionally respond with accelerated differentiation and/or lineage fate re-direction. Dr. Borghesi is an F1000 Faculty Member.