Incidence and role of antibody in graft injury: How can it best be monitored?

Alloantibodies, either preexisting or de novo developed, are associated with hyperacute, acute, and chronic rejection. Human leukocyte antigens (HLAs) are one of the major causal contributors of recipient antibody response. The average percent posttransplant antibodies specific for HLAs is 14.2% in 113 lung, 19.3% in 278 liver, 20.9% in 3,979 kidney, and 22.8% in 393 heart transplant recipients with a functioning graft. Within 1-year of follow-up, 21 of 244 (8.6%) antibody-positive patients experienced graft rejection, which is significantly higher than that found in an HLA antibody-negative patient group (43/1421*100% = 3%, P = .00003). Other polymorphic antigens such as MHC class I—related chain and endothelial cell-specific antigens are also capable of inducing antibody responses related to allograft rejection. The mechanism of antibody-mediated allograft rejection remains controversial; however, endothelial cells are considered the primary target of antibody-mediated rejection. Most pathological changes can be interpreted as a result of vascular damage and ensuing pathological compensation including tissue repair. Because alloantibody is closely correlated to rejection, we advise that posttransplant antibody be monitored. The most commonly used antibody detection techniques and their advantages and disadvantages are discussed in detail.