Phagocytic cells are a part of the innate immune system, and consist of monocyte–macrophages, polymorphonuclear leukocytes, and eosinophils. These cells mature in the bone marrow, circulate in the blood for a short time as mature cells, and enter the tissue spaces by diapedesis through capillary walls, in response to cytokines and chemotactic factors.
1. Macrophages play a central role in the innate immune response. Derived from the blood monocytes, they circulate for a few days in the blood and then leave the vascular compartment to become active tissue macrophages. Macrophages possess receptors for carbohydrates, such as mannose, that are not normally found on the cells of vertebrates. This allows the macrophages to discriminate self from nonself. Receptors for antibodies and complement are found on both neutrophils and macrophages. This adaptation allows for enhanced phagocytosis of foreign organisms coated with antibody or complement. Macrophages have the following important functions: chemotaxis (cell movement), phagocytosis (antigen engulfment), and most important of all, processing and presentation of antigen in an immunogenic form recognizable to T lymphocytes. Microorganisms engulfed by macrophages can be destroyed when they encounter a wide range of toxic intracellular molecules produced by macrophages. Some of these molecules include superoxide anion, hydroxyl radicals, hypochlorous acid, nitric oxide, plasma proteins and peptides, lysozyme, arachidonic acid metabolites, nucleotide metabolites (cyclic adenosine monophosphate), and cytokines (IL-1, IL-6, and tumor necrosis factor [TNF]). Many tissue-specific cells are of macrophage lineage and function to process and present antigen (e.g., Langerhan cells and oligodendrocytes).
2. Polymorphonuclear leukocytes originate from pluripotent bone marrow stem cells. These cells circulate in the blood and tissue, and their primary function is phagocytosis and destruction of foreign antigens. These cells function in an antigen-nonspecific fashion, and have receptors for antibodies as well as for complement, so that if microorganisms are coated with either of these components, phagocytosis will be enhanced.
3. Eosinophils, often found in inflammatory sites or at sites of immune reactivity, play a role in host defense against parasites and other large metazoan pathogens. Although eosinophils show certain functional characteristics similar to those of neutrophils, they are only weakly phagocytic. One proposed mechanism for their ability to kill parasites is via the release of cationic proteins and reactive oxygen metabolites into extracellular fluid. In addition to releasing mediators, eosinophils also possess the ability to synthesize and secrete prostaglandins, leukotrienes, and various cytokines. Eosinophils appear to have a modulatory or regulatory function in various types of inflammation. However, in the airway inflammatory response in asthma, eosinophil-derived mediators of inflammation—including major basic protein (MBP), eosinophil-derived neurotoxin (EDN), eosinophil cationic protein (ECP), and lysophospholipase (LPL)—are toxic to respiratory epithelium. Therefore, in certain instances, eosinophils promote tissue injury, and in this particular example, contribute to the pathogenesis of allergen-triggered inflammation in diseases such as asthma. The exact mechanism by which eosinophils cause oxidative damage is not known. Bromide ion is thought to be a substrate for eosinophil peroxidase, and eosinophil oxidative damage may occur via bromination of tyrosine residues.
1. Macrophages play a central role in the innate immune response. Derived from the blood monocytes, they circulate for a few days in the blood and then leave the vascular compartment to become active tissue macrophages. Macrophages possess receptors for carbohydrates, such as mannose, that are not normally found on the cells of vertebrates. This allows the macrophages to discriminate self from nonself. Receptors for antibodies and complement are found on both neutrophils and macrophages. This adaptation allows for enhanced phagocytosis of foreign organisms coated with antibody or complement. Macrophages have the following important functions: chemotaxis (cell movement), phagocytosis (antigen engulfment), and most important of all, processing and presentation of antigen in an immunogenic form recognizable to T lymphocytes. Microorganisms engulfed by macrophages can be destroyed when they encounter a wide range of toxic intracellular molecules produced by macrophages. Some of these molecules include superoxide anion, hydroxyl radicals, hypochlorous acid, nitric oxide, plasma proteins and peptides, lysozyme, arachidonic acid metabolites, nucleotide metabolites (cyclic adenosine monophosphate), and cytokines (IL-1, IL-6, and tumor necrosis factor [TNF]). Many tissue-specific cells are of macrophage lineage and function to process and present antigen (e.g., Langerhan cells and oligodendrocytes).
2. Polymorphonuclear leukocytes originate from pluripotent bone marrow stem cells. These cells circulate in the blood and tissue, and their primary function is phagocytosis and destruction of foreign antigens. These cells function in an antigen-nonspecific fashion, and have receptors for antibodies as well as for complement, so that if microorganisms are coated with either of these components, phagocytosis will be enhanced.
3. Eosinophils, often found in inflammatory sites or at sites of immune reactivity, play a role in host defense against parasites and other large metazoan pathogens. Although eosinophils show certain functional characteristics similar to those of neutrophils, they are only weakly phagocytic. One proposed mechanism for their ability to kill parasites is via the release of cationic proteins and reactive oxygen metabolites into extracellular fluid. In addition to releasing mediators, eosinophils also possess the ability to synthesize and secrete prostaglandins, leukotrienes, and various cytokines. Eosinophils appear to have a modulatory or regulatory function in various types of inflammation. However, in the airway inflammatory response in asthma, eosinophil-derived mediators of inflammation—including major basic protein (MBP), eosinophil-derived neurotoxin (EDN), eosinophil cationic protein (ECP), and lysophospholipase (LPL)—are toxic to respiratory epithelium. Therefore, in certain instances, eosinophils promote tissue injury, and in this particular example, contribute to the pathogenesis of allergen-triggered inflammation in diseases such as asthma. The exact mechanism by which eosinophils cause oxidative damage is not known. Bromide ion is thought to be a substrate for eosinophil peroxidase, and eosinophil oxidative damage may occur via bromination of tyrosine residues.
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