Opsonization of Apoptotic Cells: Implications for Uptake and Autoimmunity

Authors

  • DROR MEVORACH

    Corresponding author
    1. The Laboratory for Cellular and Molecular Immunology, Tel-aviv Medical Center, Hadassah Medical Center and the Hebrew University, Jerusalem, Israel
    Search for more papers by this author

Address for correspondence: Dror Mevorach, M.D., The Laboratory for Cellular and Molecular Immunology, Department of Medicine, Hadassah Medical Center and the Hebrew University, P.O. Box 12000, Jerusalem 91120, Israel. Voice: 972-2-0776295; fax: 972-2-643–3935. mevdm@netvision.net.il

Abstract

Abstract: As a part of innate immunity, soluble host proteins called opsonins, which include complement ligands and immunoglobulins, initially coat microorganisms that penetrate the mammalian sterile milieu. The main purpose of opsonization is to allow subsequent clearance of opsonized particles by specific receptors on the surface of leukocytes. Similarly, several proteins that may act as opsonins and have a role in uptake of apoptotic cells and bodies include thrombospondin I, the complement system, β2GPI, immunoglobulins, CRP, and some unidentified others. The surface changes that lead to opsonization include the appearance of phosphatidylserine that acts as an activator molecule for some known opsonins as the complement system and β2GPI. The consequence of altered opsonization is demonstrated by the development of autoimmunity in C1Q deficient mice, and the pro-inflammatory response by macrophages ingesting apoptotic cell opsonized by an autoantibody.

Ancillary