Authors
Yaima Tundidor Cabado, Lazaro Gil Gonzalez, Yeniley Ruiz Noa, Alequis Pavon Oro, Akash Gupta, Yulia Lin, Heather VanderMeulen, Noah Zweig, Harley Meirovich, Amie Malkin, Chantal Armali, Katrina Billingsley, Donald R Branch, Alan H Lazarus
Published in
Transfusion. Oct 26, 2026. Epub Oct 26, 2026.
Abstract
Red blood cell (RBC) alloantibodies can cause hemolytic transfusion reactions and complicate compatible blood provision. Although antibody-opsonized RBCs are thought to be cleared partly through macrophage Fcγ receptor-mediated phagocytosis, the Fcγ receptors involved in phagocytosis induced by non-D alloantibodies remain incompletely defined.
RBCs were sensitized with WHO anti-E or anti-C typing sera, or with plasma/serum from patients alloimmunized against RhE or K. Phagocytosis was assessed using THP-1-CD16A macrophages expressing FcγRI, FcγRIIA, and FcγRIII. Receptor involvement was evaluated using receptor-specific deglycosylated blocking monoclonal antibodies.
RBCs sensitized with WHO anti-E or anti-C sera, or with patient-derived anti-E or anti-K alloantibodies, were phagocytosed by THP-1-CD16A macrophages. FcγRI or FcγRIII blockade reduced phagocytosis, although the magnitude of inhibition varied by antibody source and individual patient sample. FcγRIIA blockade produced little or no significant reduction across the conditions tested. Combined FcγRI and FcγRIII blockade produced the greatest inhibition with WHO reference sera, although inhibition was not fully additive. Patient-derived anti-E and anti-K samples showed a similar pattern.
These findings support a functional contribution of FcγRI and FcγRIII to alloantibody-mediated RBC phagocytosis in this in vitro macrophage model, while suggesting a limited role for FcγRIIA under these experimental conditions.
PMID:
42928980
Bibliographic data and abstract were imported from PubMed on 26 Oct 2026.
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