The clear role of donor-specific anti-HLA antibodies (DSA) is recognized in most transplants with the sole exception of the liver. This is a classically immunologically privi-leged?rgan and it is well known that, due to their special allogeneic tolerance, liver allografts are generally transplanted with a positive cross-match (CM), with total HLA incompatibility, and even with the presence of DSAs, appearing relatively resistant to antibody mediated rejection (AMR) [1]. However, lately there has been a significant renewal of interest in HLA and non-HLA antibodies in liver transplantation (LT), with HLA and glutathione-S-transferase T1 (GSTT1) being the most relevant antigens, although also the receptor-angiotensin-type-1 (AT1R) appears to be involved in liver fibrosis. Thus, HLA-DSAs (+) have been associated with an increased risk of chronic rejection (CR) or acute rejection (AR) with ductopenia, accelerated graft fibrosis, biliary complications, worse survival, and even de novo autoimmune hepatitis, although the publications are certainly contradictory [2,3] (Fig. 1).
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