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Macrophages are diffusely scattered in the connective tissue and in liver (Kupffer cells), spleen and lymph nodes (sinus histiocytes), lungs (alveolar macrophages), and central nervous system (microglia). The half-life of blood monocytes is about 1 day, whereas the life span of tissue macrophages is several months or years.
The activation of T H 1 and M1 macrophage is a positive feedback loop, with IFN-γ from T H 1 cells upregulating CD40 expression on macrophages; the interaction between CD40 on the macrophages and CD40L on T cells activate macrophages to secrete IL-12; and IL-12 promotes more IFN-γ secretion from T H 1 cells.
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]
Overview of phagocytosis Phagocytosis versus exocytosis. 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.
Honoured as the "father of innate immunity", [16] [17] Metchnikoff was the first to discover a process of immunity called phagocytosis and the cell responsible for it, called phagocyte, specifically macrophage, in 1882.
It has been known for some time that animals defend themselves against cancer by antibody-mediated or antibody-independent phagocytosis of viable tumour cells by macrophages. Recognition of viable cancer cells for phagocytosis may be based on the expression of novel antigens, senescence markers, phosphatidylserine or calreticulin.
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.
Through the release of Interleukin 4 (IL-4) and Interleukin 13 (IL-13) by TH2, or T helper cells, and mast cells, these macrophages can fuse to form foreign body giant cells. [1] [4] The macrophages are initially attracted to the injury/infection site through a variety of chemoattractants like growth factors, platelet factors, and interleukins. [4]