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What is macrophage?


What is macrophage? 
macrophage is a type of phagocyte, which is a cell responsible for detecting, engulfing and destroying pathogens and apoptotic cells. Macrophages are produced through the differentiation of monocytes, which turn into macrophages when they leave the blood. Macrophages also play a role in alerting the immune system to the presence of invaders.

Macrophage function in detail

Phagocytosis
The term phagocytosis is formed form the Greek words "phagein" meaning to eat, "kytos" or cell and "osis" which means process. Phagocytosis is the term used to describe the engulfing and destroying of defective or microbial cells.
When inflammation occurs, monocytes undergo a series of changes to become macrophages and target cells that need eliminating. Once engulfed, cellular enzymes inside the macrophage destroy the ingested particle. Some macrophages act as scavengers, removing dead or necrotic cells while others provide host immunity by engulfing microbes
ingested microbe or dead cell is engulfed in what is called a phagosome, a vesicle which is formed around the microbe by the cell membrane. This then fuses with a lysosome, another specialized vesicle that contains digestive enzymes for disintegrating the contents of the phagosome. The fused lysosome and phagosome is referred to as a phagolysosome.
Most macrophages can live for several months and can kill hundreds of different bacteria before they die. In this way, macrophages provide a non-specific or innate immunity.
Adaptive immunity
Another function of macrophages is to alert the immune system to microbial invasion. After ingesting a microbe, a macrophage presents a protein on its cell surface called an antigen, which signals the presence of the antigen to a corresponding T helper cell.
The antigen being displayed is attached to an MHC class II molecule, which acts as a signal to other white blood cells that the marcophage is not actually a foreign invader even though it is displaying an antigen.
On identifying an antigen, the T helper cell activates other cells of the immune system such as cytotoxic T 'cells to attack the infected cell.
T helper cells also stimulate the B cells of the immune system to secrete antibodies. Each antigen has specific antibodies that are produced against it in large amounts. This "signature" antigen is also remembered by antibodies, which directly target any cells displaying the antigen in the future, should another infection occur. This developed immunity is termed adaptive or acquired immunity.
Tissue repair system in macrophage

Macrophages have frequently been reported to play divergent roles in tissue injury and tissue repair . A better understanding of these roles might be obtained by considering unique factors associated with the environmental stimulus that induces the injury, the resident tissue microenvironment in which the injury occurs, and the ontogeny of the macrophages. In addition, the role of any given macrophage population in tissue injury and repair can change dramatically with time, which might explain occasionally divergent results in the same model system. The molecular events that orchestrate the changing roles for different macrophage populations over the course of tissue injury and repair are beginning to be understood. Some of these common mechanisms are discussed below.
Macrophages as active or passive participants in tissue repair. During tissue injury, pathogens, infected cells, and cells dying from necroptosis or pyroptosis release pathogen- or damage-associated molecular patterns (PAMPs or DAMPS), which activate inflammatory signaling pathways in macrophages and other resident cell populations that recruit neutrophils, monocytes, and other inflammatory cells to the tissue. Once the acute injury has been controlled, macrophages play a role in suppressing inflammation and initiating wound repair by clearing debris and producing growth factors and mediators that provide trophic support to the tissue in which they reside  We suggest two nonexclusive pathways by which tissue macrophages might contribute to repair . The first process, which we refer to as “passive macrophage repair,” involves the progressive differentiation of monocyte-derived macrophages in response to a growing number of “normal” signals originating from the regenerating tissue microenvironment. As this process of differentiation occurs, the macrophages take on phenotype and function increasingly similar to those of homeostatic tissue-resident macrophages. The result is a positive-feedback loop in which an increasing normalization of the tissue microenvironment drives a progressively more homeostatic role for macrophages, which in turn promote tissue repair. In this model, monocyte-derived macrophages may develop a capacity for self-renewal and persist in the tissue after resolution, perhaps through downregulation of the transcription factor MAFB  Alternatively, monocyte-derived macrophages might die by apoptosis, allowing the restoration of tissue-resident macrophages through proliferation and migration, as was shown in microglia using an elegant fate-mapping system 

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