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Updated: Feb 22, 2026
Depletion of Specific Cell Populations by Complement Depletion
Published on: February 5, 2010
Complement Depletion Improves Human Red Blood Cell Reconstitution in Immunodeficient Mice
Bing Chen1, Wei Fan2, Jun Zou2
1The First Bethune Hospital and Institute of Immunology, Jilin University, Changchun 130061, China; National-Local Joint Engineering Laboratory of Animal Models for Human Diseases, Changchun 130061, China; International Center of Future Science, Jilin University, Changchun 130012, China; China-Japan Union Hospital of Jilin University, Changchun 130033, China.
Abstract:
We have previously shown that human red blood cells (hRBCs) are subject to robust rejection by macrophages in immunodeficient mice. In this study, we found that mouse serum induces hRBC adherence to murine phagocytic cells, including professional phagocytic macrophages and neutrophils and non-professional phagocytic endothelial cells. Complement was found to be responsible for mouse-serum-induced hRBC adherence to murine phagocytic cells. Although hRBC survival was not improved in NOD/SCID mice with complement depletion by cobra venom factor (CVF), CVF significantly prolonged hRBC survival in mice that were depleted of phagocytic macrophages by clodronate-liposomes. This combination treatment also synergistically improved hRBC reconstitution in human CD34+ cell-grafted mice, offering a valuable model to examine human erythropoiesis and RBC function. These data indicate that complement, which might be dispensable for hRBC rejection by macrophages, is critical in hRBC rejection by other types of murine phagocytic cells, such as neutrophils and endothelial cells.
