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, beta 2GPI, 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 beta 2GPI. 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.
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