Phagocytosis by neutrophils and monocytes

Phagocytosis by neutrophils and monocytes is a fundamental innate immune process where specialized cells identify, engulf, and destroy pathogens, apoptotic cells, and cellular debris. This complex cellular activity is initiated by the engagement of various cell surface receptors, most notably Fc gamma receptors (FcγRs) and complement receptors (CRs), which recognize targets opsonized by antibodies or complement proteins [3, 9, 12, 16]. Upon binding, the phagocyte undergoes significant cytoskeletal reorganization to internalize the target into a phagosome, which subsequently matures and fuses with lysosomes to eliminate the threat via enzymatic degradation and the production of reactive oxygen species [2, 13]. In modern pharmacology, this process is frequently targeted to improve the efficacy of monoclonal antibodies through antibody-dependent cellular phagocytosis (ADCP) or to overcome 'immune checkpoints' like the CD47-SIRPα pathway that cancer cells use to evade engulfment [4, 9]. Conversely, the suppression of phagocytic activity is a therapeutic goal in managing severe inflammatory or autoimmune conditions to prevent phagocyte-mediated tissue injury [1, 15]. Because it represents a biological process involving numerous distinct proteins rather than a single molecular entity, it is classified as a physiological phenomenon rather than a discrete drug target.

Other names

PhagocytosisOpsonophagocytosisPhagocytic activityPhagocyte effector functionCell eating

Drugs modulate this process by enhancing antibody-dependent cellular phagocytosis (ADCP), blocking inhibitory 'don't eat me' signals (e.g., CD47-SIRPα axis), stimulating the production of phagocytic cells, or suppressing phagocyte activation to reduce inflammatory damage.