David Lewinsohn
After receiving his B.S. in biology from Haverford College, David Lewinsohn attended Stanford University School of Medicine. In 1989 he received his Ph.D. in cancer biology and received his M.D. the same year. Dr. Lewinsohn was a Fellow of Pulmonary and Critical Care Medicine at the University of Washington, Seattle, WA, from 1993-1996, and a senior fellow and acting instructor from 1996-1998. During 1996-1998 he was also an investigator at the Infectious Disease Research Institute in Seattle, WA.
David Lewinsohn’s original experience in immunology focused on defining the role of the homing receptor L-selectin on neutrophil adhesion. However, since his pulmonary fellowship, he has been interested in the immune system’s ability to detect and respond to the intracellular infection with Mtb. While it is clear that CD4+ T cells play a central role in the control of mycobacterial infection, CD8+ T cells are uniquely poised to recognize those cells harboring intracellular bacteria, such that these responses can be used as a surrogate for bacterial burden and/or infection. As a result, he has focused his work on understanding the mechanisms by which human CD8+ T cells can recognize cells harboring intracellular Mtb.He has focused on human, Mtb-specific T cells, and have defined HLA alleles used to present Mtb-derived antigen, have allowed for the definition of those antigens and epitopes that are presented, and have allowed for the analysis of the mechanisms by which Mtb-derived antigens are processed and presented.
His laboratory is run jointly with Dr. Deborah Lewinsohn, who is the Division Head of Pediatric Infectious Diseases, and whose interest has been in the immunology of pediatric TB, and the mechanisms underlying the susceptibility of young children to TB. As a result, the laboratory provides a rich environment spanning basic immune mechanisms underlying the cellular immunology and cellular biology of human infection with Mtb, to translation of these observations in TB endemic regions of the world.