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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. It is one type of endocytosis. A cell that performs phagocytosis is called a phagocyte.
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]
This change is directly caused by the intestinal macrophages environment. Surrounding intestinal epithelial cells release TGF-β, which induces the change from proinflammatory macrophage to noninflammatory macrophage. [125] Even though the inflammatory response is downregulated in intestinal macrophages, phagocytosis is still carried out.
Endocytosis is a cellular process in which substances are brought into the cell. The material to be internalized is surrounded by an area of cell membrane, which then buds off inside the cell to form a vesicle containing the ingested materials. Endocytosis includes pinocytosis (cell drinking) and phagocytosis (cell eating). It is a form of ...
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.
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.
The process is tightly regulated and the inflammatory response varies depending on the particle type within the phagosome. Pathogen-infected apoptotic cells will trigger inflammation, but damaged cells that are degraded as part of the normal tissue turnover do not. The response also differs according to the opsonin-mediated phagocytosis.
The second strategy is based on the idea that autophagy is a protein degradation system used to maintain homeostasis and the findings that inhibition of autophagy often leads to apoptosis. Inhibition of autophagy is riskier as it may lead to cell survival instead of the desired cell death. [112]