Ligation of complement receptor 1 increases erythrocyte membrane deformability

Author:

Glodek Aleksandra M.1,Mirchev Rossen2,Golan David E.23,Khoory Joseph A.4,Burns Jennie M.5,Shevkoplyas Sergey S.5,Nicholson-Weller Anne16,Ghiran Ionita C.1

Affiliation:

1. Division of Allergy and Inflammation and Division of Infectious Diseases, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA;

2. Department of Biologic Chemistry and Molecular Pharmacology, Harvard Medical School, Boston MA;

3. Division of Hematology, Brigham and Women's Hospital, Boston, MA;

4. Department of Biology and Biotechnology, Worcester Polytechnic Institute, Worcester, MA;

5. Department of Biomedical Engineering, Tulane University, New Orleans, LA; and

6. Divsion of Infectious Diseases, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA

Abstract

AbstractMicrobes 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 β-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.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

Reference54 articles.

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3. Immune complexes and erythrocyte CR1 (complement receptor type 1): effect of CR1 numbers on binding and release reactions.;Ng;Clin Exp Immunol,1988

4. Immune adherence revisited: novel players in an old game.;Hess;News Physiol Sci,2003

5. The immune-adherence phenomenon. A hypothetical role of erythrocytes in defense against bacteria and viruses.;Nelson;Proc Royal Soc Med,1956

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