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