Journal
BLOOD
Volume 116, Issue 26, Pages 6063-6071Publisher
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2010-04-273904
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Funding
- National Institutes of Health [AI42987, R01HL32854]
- Medical Research and Material Command (MRMC) [W81XWH 07-1-0286]
- Defense Advanced Research Projects Agency [FA9550 08-1-0364]
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Microbes as well as immune complexes and other continuously generated inflammatory particles are efficiently removed from the human circulation by red blood cells (RBCs) through a process called immune-adherence clearance. During this process, RBCs use complement receptor 1 (CR1, CD35) to bind circulating complement-opsonized particles and transfer them to resident macrophages in the liver and spleen for removal. We here show that ligation of RBC CR1 by antibody and complement-opsonized particles induces a transient Ca++ influx that is proportional to the RBC CR1 levels and is inhibited by T1E3 pAb, a specific inhibitor of TRPC1 channels. The CR1-elicited RBC Ca++ influx is accompanied by an increase in RBC membrane deformability that positively correlates with the number of preexisting CR1 molecules on RBC membranes. Biochemically, ligation of RBC CR1 causes a significant increase in phosphorylation levels of beta-spectrin that is inhibited by preincubation of RBCs with DMAT, a specific casein kinase II inhibitor. We hypothesize that the CR1-dependent increase in membrane deformability could be relevant for facilitating the transfer of CR1-bound particles from the RBCs to the hepatic and splenic phagocytes. (Blood. 2010; 116(26):6063-6071)
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