Organ transplantation is currently one of the best methods for the treatment of end-stage organ failure. With the continuous improvement of surgical techniques and the development and application of new immunosuppressive drugs, the incidence of acute cellular rejection is gradually decreasing and the graft success rate and graft survival rate are increasing. Nevertheless, rejection is still a major factor affecting long-term functional graft survival, especially antibody-mediated humoral rejection is an important cause of chronic graft failure. Terasaki et al. proposed the humoral immune theory of organ transplant rejection in 2003 after long-term clinical and basic studies with large samples, and concluded that antibodies, especially donor-specific HLA antibodies, are an important cause of allograft rejection, and the humoral rejection theory is based on: (i) antibodies cause hyperacute rejection of renal transplantation; (ii) antibodies cause functional impairment associated with early transplantation of kidney C4d deposition on the glomerulus and peritubular capillary wall (PTC); (3) antibodies are an important indicator of acute rejection of early transplanted kidney; (4) antibodies are present in the vast majority of patients who experience renal transplant rejection; (5) antibodies are closely associated with chronic rejection not only in renal transplantation but also in heart transplantation, lung transplantation and liver transplantation; (6) antibodies in the serum often appear before transplanted kidney rejection and fine bronchial inflammatory occlusion before transplantation. The immunopathological mechanism by which antibody-mediated humoral rejection impairs graft function is as follows: graft vascular endothelial cells are the initial target for the action of allogeneic antibodies such as DSA, which, when specifically bound to the corresponding antigen on the surface of graft vascular endothelial cells, can damage vascular endothelial cells through four different pathways. (1) the antigen-antibody complex activates the complement system through the classical pathway, forming a membrane tapping complex that directly damages vascular endothelial cells; (2) the soluble complement fragments formed by the activated complement system can recruit and chemotactic inflammatory cells, leading to vascular endothelial cell injury; (3) phagocytes can bind to the complement fragments deposited on the endothelial cell surface by expressing complement fragment receptors, exerting the immunomodulatory effect of complement and damaging vascular endothelial cells; ④ Complement non-dependent antibody-mediated cytotoxicity (ADCC). The mechanism of damage to graft function in chronic humoral rejection is different from that in hyperacute rejection, mainly through the pathological process of progressive damage-repair-damage, causing continuous proliferation of vascular endothelial cells and smooth muscle cells, which in turn leads to thickening of the vessel wall, narrowing or even occlusion of the lumen, arteriosclerosis, interstitial fibrosis of renal tissue and tubular atrophy, and deposition of complement cleavage product C4d in the perinephric capillary wall. deposition in the perinephric capillary wall, resulting in progressive graft hypofunction to complete failure.