Lisa Borghesi, PhD
- Associate Professor, Department of Immunology
- Scientific Director, United Flow Core
- Member, Graduate Program in Microbiology and Immunology (PMI)
Education & Training
- PhD, University of Connecticut
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.
Liu A, Chen M, Kumar R, Stefanovic-Racic M, O'Doherty R, Ding Y, Jahnen-Dechent W and Borghesi L. 2018. Bone marrow lympho-myeloid malfunction in obesity requires precursor cell-autonomous TLR4. Nat. Comm. 8: 708.
Liu A, Wang Y, Ding Y, Baez I, Payne K and Borghesi L. 2015. Hematopoietic stem cell expansion and common lymphoid progenitor depletion requires hematopoietic-derived, cell-autonomous TLR4 in a model of chronic endotoxin. J. Immunol. (Cutting-Edge). 195: 2524-2528.
Santos P, Ding Y and Borghesi L. 2014. Cell-intrinsic in vivo requirement for the E47-p21 pathway in long-term hematopoietic stem cells. J. Immunol. 192: 160-168.
Yang Q, Esplin B and Borghesi L. 2011. E47 regulates hematopoietic stem cell proliferation and energetics but not myeloid lineage restriction. Blood. 117: 3529-3538.
Martincic K, Alkan S, Cheatle A, Borghesi L and Milcarek C. 2009. Transcription elongation factor ELL2 directs immunoglobulin secretion in plasma cells by stimulating altered RNA processing. Nature Immunol. 10: 1102-1109.