Michael Lipscomb

Interim Associate Dean for Graduate Education
Associate Professor


Dr. Lipscomb received his B.S. degree from University of California Los Angeles with a degree in Microbiology, Immunology and Molecular Genetics prior to receiving a Ph.D. degree in Immunology from the University of Pittsburgh. His postdoctoral training was at University of Pennsylvania and Children's Hospital of Philadelphia. Prior to coming to the University of Minnesota in 2022, Dr. Lipscomb held a faculty position at Howard University.

Research Summary

Research in the Lipscomb Lab employs both basic and translational approaches to delineate the immunoregulatory networks that govern antigen presenting myeloid cell development and function. Specific focus is on defining the roles of novel genes that regulate dendritic cells (DC), monocyte and macrophage intracellular signaling events that include modulation of Ca2+ and cyclic nucleotides levels, activation and inactivation of protein kinases (i.e. PKC and PKA) and downstream post-translational modifications of NFkB/ERK related pathways. The overarching objective is to significantly increase the understanding of how DC and macrophages coordinate differentiation and immunity under steady-state vs. disease settings. In a related series of studies, the Lipscomb lab investigates how antigen presenting myeloid cells contribute to autoimmune disorders, with a chief focus on delineating the pathways directing type 1 diabetes (T1D) and intestinal bowel disease (IBD). Novel genes present in the MHC class III locus within the myeloid groups are studied to determine their collective contribution to initiating, sustaining and directing autoimmune pathologies. The laboratory employs conditional and global knockout mouse models to gain mechanistic insights into in vivo functional outcomes. This is often combined with use of viral and bacterial challenge studies and antigen-restricted mouse models (i.e. OT-I, OT-II) to evaluate immune responses in an antigen-specific manner upon pathogen exposure. Similarly, autoimmune mice models (i.e. NOD and Mdr1a-/-) are employed to best describe how key gene expression in MHC class III regions regulate chronic inflammatory states and autoreactive T cell responses.

Research Interests
Myeloid cell biology
antigen presentation