Reduced graft-versus-host disease in C3-deficient mice is associated with decreased donor Th1/Th17 differentiation.

ABSTRACT: Graft-versus-host disease (GVHD) after allogeneic hematopoietic stem cell transplantation is mediated by the activation of recipient dendritic cells and subsequent proliferation of donor T cells. The complement system was recently shown to modulate adaptive immunity through an interaction of the complement system and lymphocytes. Complement proteins participate in the activation of dendritic cells, antigen presentation to T cells, and proliferation of T cells. Our studies with a murine model of bone marrow transplantation demonstrate that complement system regulates alloimmune responses in GVHD. Mice deficient in the central component of the complement system (C3(-/-)) had significantly lower GVHD-related mortality and morbidity compared with wild-type recipient mice. The numbers of donor-

SUBMITTER: Ma Q 

PROVIDER: S-EPMC3437318 | biostudies-literature | 2012 Aug

REPOSITORIES: biostudies-literature