De novo HLA Class II antibodies are associated with the development of chronic but not acute antibody-mediated rejection after liver transplantation - a retrospective study

Transpl Int. 2020 Dec;33(12):1799-1806. doi: 10.1111/tri.13763. Epub 2020 Oct 27.

Abstract

Donor-specific antibodies (DSA) cause antibody-mediated rejection (AMR); however, their pathogenic role has not yet been adequately investigated after liver transplantation. The aim of our study was to analyse the clinical significance of DSA and complement-binding DSA for the prediction of AMR after liver transplantation. Our cohort included 120 liver recipients with assessed protocol biopsies one year post-transplant. All patients had defined HLA-specific and complement-binding (C1q + and C3d+) antibodies before and in regular intervals after transplantation. The incidence of DSA was evaluated in relation with clinical and histopathological data in the liver allografts. A higher occurrence of acute AMR was observed in recipients with preformed complement-binding DSA to HLA Class I antigens. Patients who developed chronic AMR had more frequently de novo-produced antibodies against HLA Class II antigens (P = 0.0002). A correlation was also found between de novo-formed C1q + and C3d+-binding antibodies to HLA Class II antigens and the development of chronic AMR (P = 0.043). Our study implies that preformed complement-binding DSA to HLA Class I antigens are related to increased risk of acute antibody-mediated rejection, while chronic AMR is more frequent in patients with de novo-produced antibodies to HLA Class II antigens after liver transplantation.

Keywords: C4d deposits; HLA; complement-binding; donor-specific antibodies; rejection.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Complement C1q
  • Graft Rejection
  • Graft Survival
  • HLA Antigens
  • Humans
  • Isoantibodies
  • Kidney Transplantation*
  • Liver Transplantation* / adverse effects
  • Retrospective Studies
  • Tissue Donors

Substances

  • HLA Antigens
  • Isoantibodies
  • Complement C1q