Current understanding of the pathophysiology and management of acute graft versus host disease.

Abstract

The use of reduced-intensity conditioning has expanded the eligibility of hematopoietic cell transplantation (HCT) to older patients. In addition to reduced-intensity conditioning, increased availability of alternative donors including HLA mismatched unrelated donors have improved the safety as well as access of allogeneic HCT for a larger number of patients. However, acute graft versus host disease (GVHD) remains a lethal complication even in HLA - matched donor - recipient pairs and there is currently no standard treatment of patients with steroid refractory GVHD. The pathophysiology of GVHD fundamentally depends upon aspects of adaptive immunity and interactions between donor T cells and host dendritic cells. Recent work has revealed that the role of other immune cells or endothelial cells and components of the innate immune response are also important. Based on understanding of the pathophysiology of acute GVHD, multitarget therapy and cell therapy may open a new area for future therapeutic approaches.