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Phagocytosis (from Ancient Greek φαγεῖν (phagein) 'to eat' and κύτος (kytos) 'cell') is the process by which a cell uses its plasma membrane to engulf a large particle (≥ 0.5 μm), giving rise to an internal compartment called the phagosome.
Unbound phagocyte surface receptors do not trigger phagocytosis. 2. Binding of receptors causes them to cluster. 3. Phagocytosis is triggered and the particle is taken up by the phagocyte. Phagocytosis is the process of taking in particles such as bacteria, invasive fungi, parasites, dead host cells, and cellular and foreign debris by a cell. [22]
Phagocytosis of an otherwise-viable cell may occur because the cell is recognised as stressed, activated, senescent, damaged, pathogenic or non-self, or is misrecognised. Cells are phagocytosed as a result of: i) expressing eat-me signals on their surface, ii) losing don’t-eat-me signals, and/or iii) binding of opsonins .
The first demonstration of phagocytosis as a property of leukocytes, the immune cells, was from the German zoologist Ernst Haeckel. [14] [15] In 1846, English physician Thomas Wharton Jones had discovered that a group of leucocytes, which he called "granule-cell" (later renamed and identified as eosinophil [16]), could change shape, the phenomenon later called amoeboid movement.
Antibody opsonization is a process by which a pathogen is marked for phagocytosis through coating of a target cell with antibodies. Immunoglobulins participate in molecular tagging of pathogens which display antigens recognised by their specific paratope.
Due to their role in phagocytosis, macrophages are involved in many diseases of the immune system. For example, they participate in the formation of granulomas, inflammatory lesions that may be caused by a large number of diseases. Some disorders, mostly rare, of ineffective phagocytosis and macrophage function have been described, for example ...
The process of phagocytosis showing phagolysosome formation. Lysosome(shown in green) fuses with phagosome to form a phagolysosome. Membrane fusion of the phagosome and lysosome is regulated by the Rab5 protein, [1] a G protein that allows the exchange of material between these two organelles but prevents complete fusion of their membranes. [1]
Opsonins induce phagocytosis of targets by binding the targets (e.g. bacteria) and then also binding phagocytic receptors on phagocytes. Thus, opsonins act as bridging molecules between the target and the phagocyte, bringing them into contact, and then usually activating the phagocytic receptor to induce engulfment of the target by the phagocyte.