The pathophysiology of<unk> D includes three phases: # The afferent phase: activation of APC (antigen presenting cells) # The efferent phase: activation, proliferation, differentiation and migration of effector cells # The effector phase: target tissue destruction Activation of APC occurs in the first stage of<unk> D. Prior to haematopoietic stem cell transplantation, radiation or chemotherapy results in damage and activation of<unk>  tissues, especially intestinal mucosa. This allows the microbial products to enter and stimulate pro-inflammatory cytokines such as IL-1 and TNF-α. These proinflammatory cytokines increase the expression of MHC and adhesion molecules on APCs, thereby increasing the ability of APC to present antigen. The second phase is characterized by the activation of effector cells. Activation of donor T-cells further enhances the expression of MHC and adhesion molecules, chemokines and the expansion of CD8 + and CD4 + T-cells and guest B-cells. In the final phase, these effector cells migrate to target organs and mediate tissue damage, resulting in multiorgan failure.
Graft-versus-host disease
Transplant rejection
Cardiac allograft vasculopathy
Vasculogenic mimicry
Infectious tolerance
Disseminated disease
Chronic allograft nephropathy
Post-transplant lymphoproliferative disorder