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Research Faculty > Brian Wilson, MD


Brian Wilson, MD

Assistant Progressor of Medicine, Harvard Medical School
65 Landsdowne Street
Cambridge, MA 02139

Brian_Wilson@dfci.harvard.edu


 

Dr. Wilson completed clinical training in Internal Medicine and Infectious Diseases at the MGH, and postdoctoral research training in the Department of Cellular & Molecular Biology, Harvard University. Currently, Dr. Wilson is an Assistant Professor of Medicine at Harvard Medical School in the Diabetes Unit at the MGH.

He is the recipient of many awards including: Infectious Disease Society of America Medical Student Research Award, American Cancer Society Joseph S. Silber Student Fellow award, election to the Alpha Omega Alpha Medical Honor Society, recipient of the Max Miller Award for Excellence in Medicine, CWRU School of Medicine, and a Daland Fellow, or the American Philosophical Society.

Dr. Wilson's research focuses on the molecular mechanism by which CD1d-restricted T cells (iNKT) are key players in controlling the autoimmune attack that results in type 1 diabetes. Investigations in the laboratory combine functional studies of iNKT cells derived from human patients with type 1 diabetes with in vivo studies of a mouse model of diabetes, the nonobese diabetic (NOD) mouse. In contrast to human type 1 diabetes, in the NOD model diabetes is relatively restricted to female mice. Both human patients with type 1 diabetes and female NOD mice have a paucity of iNKT cells, and those that are present are dysfunctional. To study the role of iNKT cells in the NOD mouse, the CD1d molecule was genetically deleted to generate mice that do not have any iNKT cells. As predicted, the deletion of CD1d exacerbated diabetes in NOD female mice. Furthermore, NOD male mice who have a low incidence of diabetes have an increased frequency of iNKT cells. Moreover, administration of a-galactosylceramide, a potent activator of iNKT cells prevented the development of diabetes in NOD female mice. A major mechanism by which iNKT cells prevent diabetes in NOD mice is by recruiting a second type tolerogenic cell, myeloid dendritic cells (DC), to the site of ongoing autoimmune attack. Strikingly, injection of NOD female mice with these DC completely prevented diabetes. Thus, the immunoregulatory role of iNKT cells occurs by recruitment of tolerogenic myeloid DC and the inhibition of ongoing autoimmune inflammation.

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