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How the Phagocytosis Occurs in Macrophages and Neutrophils and How the Remaining Antigens Reach the Lymph

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Every day we are alive, humans encounter potentially harmful disease causing organisms, or “pathogens”, like bacteria or viruses. Yet most of us are still able to function properly and live life without constantly being sick. That’s because the human body requires a multilayered immune system to keep it running smoothly. The two main classes of the immune system are the innate immune system and the adaptive immune system, or “acquired immunity”. In this article, we’ll discuss the first line of defense: the innate immune system.

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Phagocytosis is the process by which a cell takes in particles such as bacteria, parasites, dead host cells, and cellular and foreign debris. It involves a chain of molecular processes. Phagocytosis occurs after the foreign body, a bacterial cell, for example, has bound to molecules called “receptors” that are on the surface of the phagocyte. The phagocyte then stretches itself around the bacterium and engulfs it. Phagocytosis of bacteria by human neutrophils takes on average nine minutes to occur. Once inside the phagocyte, the bacterium is trapped in a compartment called a phagosome. Within one minute the phagosome merges with either a lysosome or a granule, to form a phagolysosome. The bacterium is then subjected to an overwhelming array of killing mechanisms and is dead a few minutes later. Dendritic cells and macrophages, on the other hand, are not so fast, and phagocytosis can take many hours in these cells. Macrophages are slow and untidy eaters; they engulf huge quantities of material and frequently release some undigested material back into the tissues. This debris serves as a signal to recruit more phagocytes from the blood. Phagocytes have voracious appetites; scientists have even fed macrophages with iron filings and then used a small magnet to separate them from other cells. All phagocytes, and especially macrophages, exist in degrees of readiness. Macrophages are usually relatively dormant in the tissues and proliferate slowly. In this semi-resting state, they clear away dead host cells and other non-infectious debris and rarely take part in antigen presentation. But, during an infection, they receive chemical signals—usually interferon gamma—which increases their production of MHC II molecules and which prepares them for presenting antigens. In this state, macrophages are good antigen presenters and killers

However, if they receive a signal directly from an invader, they become “hyperactivated”, stop proliferating, and concentrate on killing. Their size and rate of phagocytosis increases—some become large enough to engulf invading protozoa. In the blood, neutrophils are inactive but are swept along at high speed. When they receive signals from macrophages at the sites of inflammation, they slow down and leave the blood. In the tissues, they are activated by cytokines and arrive at the battle scene ready to kill.When an infection occurs, a chemical “SOS” signal is given off to attract phagocytes to the site. These chemical signals may include proteins from invading bacteria, clotting system peptides, complement products, and cytokines that have been given off by macrophages located in the tissue near the infection site. Another group of chemical attractants are cytokines that recruit neutrophils and monocytes from the blood. To reach the site of infection, phagocytes leave the bloodstream and enter the affected tissues. Signals from the infection cause the endothelial cells that line the blood vessels to make a protein called selectin, which neutrophils stick to when they pass by. Other signals called vasodilators loosen the junctions connecting endothelial cells, allowing the phagocytes to pass through the wall. Chemotaxis is the process by which phagocytes follow the cytokine “scent” to the infected spot. Neutrophils travel across epithelial cell-lined organs to sites of infection, and although this is an important component of fighting infection, the migration itself can result in disease-like symptoms. During an infection, millions of neutrophils are recruited from the blood, but they die after a few days.

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All MHC molecules work in the same basic way, as a scaffold to present antigen, but as a species we have in our heritage a repository of many different MHC molecules (1122 common and well-documented different alleles as of 2013). This diversity at the level of the population of all humans, is narrowed down in the individual, who inherits about nine MHC molecules at random from their parents. Your own MHC molecules define your tissue type which is the major barrier to successful organ transplantation, and the reason we keep records of the tissue type of potential donors. The chance of meeting a stranger who shares the same MHC molecules as you is tiny, which is why, among a panel of 20 million potential donors, 2–5% of individuals will not find an exact match (Paul W.E. , 2015). Even an individual with the commonest set of HLA genes found in the U.K., who needed a transplant, would only find a few hundred potential donors among this panel. This is also why your best chance of finding a compatible donor is searching among your close relatives, with whom you share genes. Of course, the complexity of this system did not arise to frustrate transplant surgeons. The immune system uses it, because each of these many different MHC molecules presents a unique selection of antigens processed from the same underlying proteins. For example, the antigens that are presented from the liver of one person will be different from the antigens presented from the liver of an unrelated person. In this way, the representation of self established by an individual's MHC, presenting its self-proteins to its own lymphocytes, is a very private system of identification that is difficult to copy, allowing the immune system to discriminate between foreign tissue transplants, invading infections and cancerous cells

Cancer can also be treated by exploiting the immune response. One early strategy for successful immunotherapy for cancer used monoclonal antibodies that blocked receptors which the tumour cells used to receive growth-promoting signals. These treatments are beneficial when the cancer cells express these receptors, but their impact is generally of only a limited duration and is eventually followed by a relapse (Abbas A.K., 2016although macrophages do not have the remarkable migratory behavior of DCs, there are some conditions such as during solid tumor growth where considerable numbers of tissue macrophages may reach and modify draining LNs. This is because, similar to the way that viruses live many lifetimes to that of a human, a growing cancer is a fast-evolving threat to health. Cancers arise when mutations that permit unrestrained growth develop, and this growth is associated with much less reliable checking of genetic fidelity. Modern techniques have allowed researchers to develop family trees based on mutations in a cancer's genes, showing how they consist of related lineages of cells that peel off from the parental line and expand through time. Every mutation that develops is an opportunity for the immune system to push back, by recognizing tumour antigens on their surface in their MHC molecules. If this mechanism were failsafe, tumours would never progress beyond this stage. But cancer can escape the immune system by deploying a number of mechanisms that shut the immune responses down. Understanding how this occurs has stimulated the development of a number of new therapies that are having an astonishing impact against some types of cancer.

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Generally speaking, although macrophages do not have the remarkable migratory behavior of DCs, there are some conditions such as during solid tumor growth where considerable numbers of tissue macrophages may reach and modify draining LNs. To properly characterize LN macrophages, and their relatives in the spleen, improved procedures for their isolation to high purity are needed. Methods that allow their culture will also greatly enhance their study. New insights into their biology are also likely to emerge from a more complete assessment of their developmental pathway(s) and relationships to other macrophage populations in the body.

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Abbas A.K., Lichtman A.H., Pillai S. Basic Immunology: Functions and Disorders of the Immune System. Amsterdam: Elsevier; 2016.

Davis D.M. The Compatibility Gene. London: Penguin; 2013.

Foster W.D. A History of Medical Bacteriology and Immunology. London: Heinemann; 1970.

Paul W.E. Immunity. Baltimore: Johns Hopkins University Press; 2015.

Silverstein A.M. A History of Immunology. Cambridge, MA: Academic Press; 1989

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