The Mitchell laboratory conducts research at the interface of immunology and vascular cell biology. Focusing on the mechanisms underlying acute and chronic rejection in solid organ allografts, the work involves mouse transplant models, as well as human clinical transplantation, focusing on understanding specific immunologic pathways that drive rejection and ultimately graft failure. The laboratory is particularly interested in the mechanisms that induce the process of allograft arteriopathy whereby allograft vessels become progressively more occluded until the grafts suffer irreversible ischemic injury. The research may have much broader applicability, since the inflammatory mediators that drive the occlusive process in transplants may also be involved in mediating the vascular wall thickening that characterizes more “typical” atherosclerosis. The laboratory uses several different strains of genetically engineered mice, deficient either in cell surface molecules that promote the cellular cross-talk necessary to promote rejection, or lacking particular cytokine or chemokine mediators or their receptors. In collaboration with other members of the Harvard and MIT communities, as well as industry (Schering-Plough, Bristol Myers-Squibb, and Novartis) the group has also evaluated promising interventions to prevent allograft arteriop.

Pathology and Health Sciences and Technology immunology and vascular cell biology grafts suffer irreversible ischemic injury.