Surface Distribution and Pathway of Internalization of C3b Receptors (CR1) in Human Neutrophils
Neutrophils are implicated in the prevention of bacterial infection. To that end, phagocytes must first sense the presence of bacteria, reach the sites of infection and eventually get in close contact with the microorganisms to ingest them (Elsbach P and Weiss J, 1988). This complex process requires the cooperation of several classes of receptors (adherence, chemoattractants, and phagocytic receptors) present on their surface. Chemoattractant receptors, which bind molecules such as C5a or fMLP, are coupled to phosphoinositide hydrolysis which leads to an increase of cytosolic free calcium [Ca2+]i and activation of protein kinase C (Snyderman R et al., 1986). In turn, this signalling cascade is thought to be essential for triggering oriented locomotion and secretion of neutrophils (Stossel TP, 1988). Among phagocytic receptors, those for Fc portion of immunoglobulins are endowed with the intrinsic ability to trigger ingestion and metabolic responses towards antibody coated particles. On the other hand, complement receptors such as CR1 (receptors for C3b), promote the binding of complement activating particles (such as bacteria or immune complexes), and their subsequent phagocytosis, synergestically with Fc receptors (Unkeless JC and Wright SD, 1988). In the case of CR1, the aquisition of the phagocytic capability requires its activation by a process thought to involve phosphorylation of the receptor (Changelian PS and Fearon DT, 1986). Full phagocytic capacity of CR1 is obtained when neutrophils are costimulated with fibronectin or laminin (Pommier et al.,1983; Bohnsack et al. 1985). Pharmacological agents such as PMA also mimic this activation process (Kazatchkine MD and Fearon DT, 1990).
KeywordsComplement Receptor Inflammation Basic Principle Cytosolic Free Calcium Phagocytic Receptor Chemoattractant Receptor
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