The pathophysiology of GvHD is based upon immune activation and inflammation due to donor-derived T cell responses, ultimately resulting in host organ damage. Acute and chronic GvHD has slightly different pathophysiologic mechanisms. The pathophysiology begins with tissue damage from the preparative regimen, then ensues with donor T cell activation, followed by destruction of host tissue in the skin, liver, and/or GI tract. Various T cell subsets play different roles in the pathophysiology of GvHD, and Th1 cells are thought to be major contributors to the inflammation and destruction that underlies the pathophysiology of GvHD.
Graft-versus-host disease pathophysiology
Allergy pathophysiology
Cardiac allograft vasculopathy pathophysiology
Cellulitis pathophysiology
Gangrene pathophysiology
Hamman-Rich syndrome pathophysiology
Graft-versus-host disease risk factors
Graft-versus-host disease causes