Open AccessCD47 blockade reduces the pathologic features of experimental cerebral malaria and promotes survival of hosts with Plasmodium infection
Author(s) -
Laughing Bear Torrez Dulgeroff,
Miranda S. Oakley,
Michal Caspi Tal,
Ying Ying Yiu,
Joy Q. He,
Maia Shoham,
Victoria Majam,
Winter A. Okoth,
Pallavi Malla,
Sanjai Kumar,
Irving L. Weissman
Publication year - 2021
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.1907653118
Subject(s) - cerebral malaria , cd47 , malaria , blockade , phagocytosis , plasmodium falciparum , case fatality rate , immunology , plasmodium berghei , medicine , monoclonal antibody , disease , macrophage , antibody , biology , receptor , biochemistry , epidemiology , in vitro
Significance Novel therapies are urgently needed that can ameliorate the clinical syndromes of cerebral malaria, the most severe consequences ofPlasmodium infection, and thereby reduce malaria fatality. Monoclonal antibodies that target CD47, a “don’t eat me” signal, have been demonstrated to enhance cellular clearance of cancer cells by promoting macrophage phagocytosis. We sought to adopt this therapeutic strategy to ameliorate the clinical syndromes associated with cerebral malaria with the goals of reducing disease-associated morbidity and mortality. We demonstrate that CD47 blockade by anti-CD47 injection leads to survival from cerebral malaria in mice.