Phagocytosis: Enhancement

Abstract

Abstract Phagocytosis is the process of cellular engulfment of particles. Professional phagocytes, such as macrophages, neutrophils and dendritic cells, are the most efficient at mediating particle ingestion though nonprofessional phagocytes, such as fibroblasts and epithelial cells, can ingest neighbouring dying cells. Pathogen ingestion for killing and antigen processing for presentation are important components of innate and acquired immunity, and removal of dying cells is critical for tissue homeostasis. The uptake of pathogens, tissue debris or apoptotic cells may be enhanced by coating the particle with host molecules called opsonins, which allow the recognition and subsequent ingestion of the particles by phagocytic receptors. There are numerous opsonins, including complement‐derived proteins such as iC3b and immunoglobulin G, which are recognised by specialised receptors including complement receptor type 3 and FcγR. The failure of efficient uptake of particles and apoptotic cell debris can have deleterious effects on the host such as leading to the spread of infection and the generation of autoimmune conditions, such as systemic lupus erythematosus (SLE). CR3 and FcγR are the most studied of the opsonic phagocytic receptors. Key Concepts Phagocytic receptors can recognise their particle by either direct binding or indirectly after it is coated with host molecules called opsonins. Professional phagocytic cells, such as dendritic cells, monocytes and macrophages, express numerous receptors capable of mediating particle ingestion. Enhanced phagocytic uptake of pathogens and dying cells is mediated by a number of overlapping opsonins and phagocytic receptors. Ingested particles are recognised by a number of different receptors which may cooperate with each other to modulate their function/activity. Though multiple receptors can mediate phagocytosis, there are subtle differences in their signalling and cell biology that can result in different cellular outcomes downstream of uptake. Removal of apoptotic cells by professional phagocytes typically results in the release of antiinflammatory mediators, while phagocytosis of pathogens can cause inflammation. Defects in the removal of both pathogens and apoptotic cells can lead to increased susceptibility to infection and autoimmune diseases.