Nature communications · 2021
Red blood cell mannoses as phagocytic ligands mediating both sickle cell anaemia and malaria resistance.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Cao Huan, Antonopoulos Aristotelis, Henderson Sadie, Wassall Heather, Brewin John, Masson Alanna, Shepherd Jenna, Konieczny Gabriela, Patel Bhinal, Williams Maria-Louise, Davie Adam, Forrester Megan A, Hall Lindsay, Minter Beverley, Tampakis Dimitris, Moss Michael, Lennon Charlotte, Pickford Wendy, Erwig Lars, Robertson Beverley, Dell Anne, Brown Gordon D, Wilson Heather M, Rees David C, Haslam Stuart M, Alexandra Rowe J, Barker Robert N, Vickers Mark A
Аннотация
In both sickle cell disease and malaria, red blood cells (RBCs) are phagocytosed in the spleen, but receptor-ligand pairs mediating uptake have not been identified. Here, we report that patches of high mannose N-glycans (Man5-9GlcNAc2), expressed on diseased or oxidized RBC surfaces, bind the mannose receptor (CD206) on phagocytes to mediate clearance. We find that extravascular hemolysis in sickle cell disease correlates with high mannose glycan levels on RBCs. Furthermore, Plasmodium falciparum-infected RBCs expose surface mannose N-glycans, which occur at significantly higher levels on infected RBCs from sickle cell trait subjects compared to those lacking hemoglobin S. The glycans are associated with high molecular weight complexes and protease-resistant, lower molecular weight fragments containing spectrin. Recognition of surface N-linked high mannose glycans as a response to cellular stress is a molecular mechanism common to both the pathogenesis of sickle cell disease and resistance to severe malaria in sickle cell trait.