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Personalized Peptide Arrays for Detection of HLA Alloantibodies in Organ Transplantation
Published on: September 6, 2017
Passenger Lymphocyte Syndrome With Multiple Allo- and Autoantibodies Following Liver Transplantation: A Case Report
Ivica Marić1,2, Tobia Gomilšek2, Klara Železnik1
1Slovenian Institute for Transfusion Medicine, Ljubljana, Slovenia.
Background:
Passenger lymphocyte syndrome (PLS) is a rare immune-mediated haemolytic complication of solid organ transplantation caused by donor-derived lymphocytes producing antibodies against recipient red blood cell (RBC) antigens. Multiple alloantibodies and concomitant autoantibody formation are uncommon, particularly in ABO-identical liver transplantation.
Case Presentation:
A 56-year-old male underwent ABO-identical but D- and Kell-non-identical liver transplantation. Approximately, 3 weeks posttransplantation, haemoglobin decreased to 81 g/L, and indirect antiglobulin testing identified anti-D and anti-E antibodies, while direct antiglobulin testing confirmed IgG-coated RBCs. Subsequently, anti-K alloantibodies and transient pan-reactive IgG autoantibodies were detected, resulting in positive crossmatches and complicated transfusion support. Because most transfused RBC units before antibody detection were D+, E+ and K+, anti-E was interpreted as probable recipient-derived transfusion-associated alloimmunisation, whereas anti-D and anti-K were consistent with donor-derived PLS. Transfusion support was subsequently restricted to D-, E- and K- RBC units. The patient remained clinically stable despite haemoglobin decline with serologic evidence of immune-mediated RBC sensitization consistent with PLS. During 4 years of follow-up, anti-D and anti-K antibodies disappeared, while only weak residual anti-E reactivity persisted.
Discussion:
The simultaneous occurrence of donor-derived alloantibodies, probable recipient-derived alloimmunisation and transient pan-reactive autoantibodies suggests broader posttransplant humoral immune activation than typically observed in classical PLS. Although clinically significant autoimmune haemolytic anaemia did not develop, the coexistence of multiple antibody specificities substantially complicated serologic interpretation and transfusion management.
Conclusion:
This case highlights complex posttransplant humoral immune dysregulation involving donor-derived alloantibodies, probable recipient alloimmunisation and transient autoantibody formation after ABO-identical liver transplantation. The coexistence of multiple antibodies significantly complicated serologic testing and transfusion support.

