INTRODUCTION

Phagocytosis, an essential component of the innate immune response, is a complex process whereby extracellular particles of diameter ≥ 0.5μm are internalized into a specialized membrane-bound vacuolar compartment. Following particle engulfment the resulting vacuoles, better known as phagosomes, undergo a maturation sequence involving fusion and fission events with components of the endocytic pathway. The resulting hybrid compartments, termed phagolysosomes, acquire the molecular machinery necessary to destroy the ingested pathogens.

The process of internalization can be envisaged as involving five distinct steps, beginning with particle recognition, receptor signaling, membrane remodeling and actin polymerization allowing for pseudopod extension, and climaxing with particle uptake into the cytosol. Although the mechanism of internalization is largely conserved among phagocytic cell types, the purpose of phagocytosis is diverse. Unicellular organisms such as amoebae engulf bacteria to obtain nutrients. In mammalian cells, neutrophils and macrophages employ phagocytosis to prevent the spread of infectious agents, but the same process is also employed for the clearance of apoptotic bodies.

Phagocytosis is a receptor-mediated event initiated by ligand recognition and particle binding. Multiple receptors recognize and prompt the elimination of the varied army of pathogenic organisms; a different set of receptors is needed to identify and clear apoptotic bodies. Indeed, the former elicit an immune and inflammatory response, whereas the latter do not.

The objective of this review is to summarize succinctly the current knowledge of the events that lead to phagocytosis.