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David  Briscoe, MD, BCh

Department: Nephrology
Research Centers: Nephrology Research Center
Hospital Title: Senior Associate in Medicine; Director, Fellowship Training Program
Academic Title: Associate Professor of Medicine, Harvard Medical School
Research Area: Transplant rejection

Research Overview

Research in the laboratory relates to the intragraft microvironment, and how it functions to both promote and inhibit the rejection process. Our studies focus on three broad areas including 1) immune-mediated angiogenesis and how angiogenesis factors function in the rejection process 2) how leukocyte-endothelial cell interactions and products of these interactions promote, sustain or inhibit T cell activation and allorecognition, and 3) whether persistent events within the microvasculature are associated with, or mediate chronic allograft rejection. We are currently expanding our research effort into the area of inflammation resolution, and we are specifically interested in endogenous mechanisms and regulatory signaling networks of pro-resolution. Understanding these processes will allow us to develop new paradigms for anti-rejection therapeutics following transplantation.

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About David Briscoe

David Briscoe is an Associate Professor at Harvard Medical School and Director of the Transplant Research Program at Boston Children’s Hospital. He is also an elected member of the National Physician-Scientist Honors Society, the American Society of Clinical Investigation (ASCI). Research in the Briscoe Laboratory focuses on intragraft mechanisms of allograft rejection, and specifically how lymphocytes and monocytes interact with the vascular endothelium in the course of cell-mediated immune inflammatory reactions. Ongoing research projects address questions about endogenous signaling within the vascular endothelial cell that both inhibit and promote inflammation and how angiogenesis is associated with chronic allograft rejection. The laboratory also has an interest in how VEGF functions in inflammation, and how VEGFR interactions and signals alter T cell activation responses. The ultimate goal of our research is to understand the complexity of chronic allograft rejection and to identify molecules and/or targets that have therapeutic potential to inhibit alloimmune-mediated graft injury.

http://www.briscoelab.com/

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