Dr. Reed's research efforts focus on understanding the mechanism of allograft injury. The development of donor specific HLA antibodies (DSA) following transplantation is associated with transplant vasculopathy, a manifestation of chronic allograft rejection leading to graft loss. Reed and her colleagues have shown that HLA DSA are pathogenic in chronic rejection by binding to HLA class I and class II molecules on endothelium of the allograft and transducing intracellular signaling pathways that stimulate cell activation, proliferation, migration and leukocyte recruitment. These studies suggest HLA DSA can play a key role in the initiation of proliferative signals and inflammation in the graft, which stimulate the development of transplant vasculopathy associated with chronic rejection of human allografts. Current efforts focus on elucidating the HLA class I and class II signal transduction pathways. Understanding these mechanisms will permit the development of new therapeutic modalities for the treatment and prevention of transplant vasculopathy and the extension of functional life of transplanted organs. The Reed lab also studies ischemia reperfusion injury (IRI) in liver transplantation, a common consequence of the transplant process. The cellular damage triggered by IRI leads to primary graft non-function, necessitating re-transplantation or leading to recipient death. IRI also predisposes the recipient to both acute and chronic rejection and graft loss. The lab is identifying the continuum of innate and adaptive immune responses mediating IRI, which will ultimately permit the development of therapeutic interventions against IRI and improve liver transplant outcomes. An additional focus of Dr. Reed's research is in the development of novel methods for immunologic assessment of the immune response to infectious pathogens in transplant patients. She and her associates are using high throughput genomics and immunomics techniques to study cytomegalovirus (CMV), a common herpes virus that can damage transplants and devastate immunocompromised patients. Approaches for improved understanding and subsequent harnessing of the host immune response to CMV are needed to reduce the burden of CMV complications in immunocompromised individuals, including chronic injury of the transplanted organ.