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Role of Mast Cells
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Mast cells, derived from hematopoietic precursors, are found predominantly near blood vessels, nerves, and subepithelial sites, where local immediate hypersensitivity reactions tend to occur12,13 These cells can be activated during acute reactions such as allergies through their highaffinity receptors for the Fc portion of immunoglobulin E (IgE) and by several
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TABLE 35-1 In ammatory-Associated Cytokines INFLAMMATORY CYTOKINE IL-1 ( and ) SECRETED BY Monocytes Macrophages B cells Dendritic cells Endothelial cells TARGET CELL OR TISSUE TH cells B cells Natural Killer (NK) cells Endothelial cells Hepatocytes Hypothalamus B cells Plasma cells Hepatocytes Neutrophils Macrophages T cells B cells Hepatocytes Macrophages In ammatory cells In ammatory cells B cells T cells NK cells Neutrophils ACTIVITY Targets a wide variety of cells to induce many in ammatory reactions: activation of TH cells; maturation and clonal expansion of B cells; enhancement of the activity of NK cells; production of other cytokines; endothelial gene regulation (increasing the expression of adhesion molecules); chemotaxis of macrophages and neutrophils; leukocyte adherence, synthesis of acute-phase-proteins by the liver; induction of fever Promotes the terminal differentiation of B cells into plasma cells; stimulates antibodies secretion by plasma cells; induces synthesis of acute-phase proteins Potent chemokine, induces adherence to endothelium and extravasation to tissues Also called cytokine synthesis inhibitory factor because it suppresses cytokine production by activated TH1 cells Stimulation of T cell-dependent B cell immunoglobulin secretion; increased platelet production; induction of IL-6; acute phase protein secretion Enhances the activity of macrophages, mediates effects important in delayed type hypersensitivity Shares several proin ammatory properties with IL-1 Induces cytokine secretion Important role in chronic in ammation Inhibits T cell and NK cell proliferation and activation; attracts monocytes to the site of in ammation; enhances cell adhesion Participates in acute in ammation
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Monocytes Macrophages TH2 cells Macrophages Endothelial cells TH2 cells Bone marrow stromal cells Some broblasts TH1 cells Cytotoxic T cells NK cells Macrophages NK cells Platelets Macrophages Lymphocytes Mast cells Macrophages T cells
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COSMETIC DERMATOLOGY: PRINCIPLES AND PRACTICE
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Granulocyte colonystimulating factor (G-CSF)
role in allergic inflammation mostly occurs through the H1-receptor18,19 Through this receptor, histamine plays a proinflammatory role by inducing the release of cytokines and lysosomal enzymes from macrophages and the expression of cell adhesion molecules18,19 Additionally, it influences the activity of basophils, eosinophils, and fibroblasts, causing smooth muscle contraction20 Although most of the effects of histamine in inflammatory allergic disease occur through the H1-receptor, cutaneous itch may occur through both the H1- and H3-receptors21
Role of Free Radicals
Oxygen-derived free radicals may be released extracellularly from leukocytes after exposure to pathogens, chemokines, and immune complexes, or following a phagocytic challenge22 The physiologic function of these reactive oxygen intermediates is to destroy phagocytized microorganisms Their production depends on the activation of the nicoti-
namide adenine dinucleotide phosphate (NADPH) oxidative system, which is a membrane-bound enzyme complex This system can be found in the plasmatic membrane as well as in the membrane of phagosomes inside the cells Superoxide anion (O2 ), hydrogen peroxide (H2O2), and hydroxyl radical (OH) are the major species produced within the cell; these metabolites can combine with nitric oxide (NO) to form other reactive nitrogen intermediates23 (see 34) Extracellular release of low levels of these potent mediators can increase the expression of chemokines, cytokines, and endothelial leukocyte adhesion molecules, amplifying the cascade that elicits the inflammatory response At higher levels, the release of these mediators can induce endothelial cell damage, which results in increased vascular permeability, neutrophil degranulation, and inactivation of antiproteases, such as 1-antitrypsin, leading to increased destruction of the extracellular matrix24 Serum, tissue fluids, and host cells all possess antioxidant mechanisms that pro-
tect against these potentially harmful oxygen-derived radicals These include among others: (1) the copper-containing serum protein ceruloplasmin; (2) the iron-free fraction of serum, transferrin; (3) the enzyme superoxide dismutase, which is found or can be activated in various cell types; (4) the enzyme catalase, which detoxifies H2O2; and (5) glutathione peroxidase, another powerful H2O2 detoxifier The influence of oxygen-derived free radicals in any given inflammatory reaction will always depend on the balance between the production and the inactivation of these metabolites by both cells and tissues
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