CROSS TALK BETWEEN ALLOIMMUNE RESPONSE TO HLA AND AUTOIMMUNITY IN PATHOGENESIS OF CHRONIC REJECTION IN LUNG TRANSPLANTATION

摘要

Chronic rejection remains the leading cause of long-term allograft failure in transplant recipients (slide 2). Several risk factors have been proposed to play a role in chronic rejection, including recurrent/refractory acute rejections, CMV and other viral infections, human leukocyte antigen (HLA) mismatches, organ ischemia etc. Several non-specific risk factors such as donor and recipient age, graft ischemic time, primary graft dysfunction and bacterial/fungal/non-CMV viral infection have also been associated with decreased long term survival of the transplanted organ (slide 3). The hallmark of chronic rejection is fibrosis of graft parenchyma developing over months to years. The pathogenesis of chronic rejection is initiated by a host-anti-graft-immune response. Both immune (antigen-dependent) and non-immune (antigen-independent) factors lead to fibroproliferative changes that cause occlusion of tubular structures in the allograft. This is characterized by terminal airway obliteration in lung allografts, focal cellular interstitial infiltration and glomerulosclerosis in renal allografts, and coronary arteriopathy in cardiac allografts.