NeutrophilandItsSurfaceMolecules

Neutrophils are important phagocytotic leukocytes (white blood cells) that internalize and destroy infectious bacteria by a respiratory burst of reactive oxygen species and by enzymatic digestion. Along with macrophages, neutrophils are crucial phagocytotic cells of the immune system and also contribute to anti-viral defenses, binding to and eliminating free virus or virus-infected cells. The presence of cytoplasmic granules in neutrophils leads to their classification as granulocytes, along with basophils and eosinophils. A lack of neutrophils or their normal function causes a variety of immune disorders and measuring neutrophil cell surface proteins can diagnose abnormal immune function. One such disorder is caused by a lack of normal expression of the adhesion molecules CD11 and CD18 by neutrophils, preventing them from interacting normally with adhesion molecules on endothelial cells and migrating into inflamed sites in tissues. CD11a and CD18 together form the LFA-1 receptor for ICAM-1 on endothelial cells and CD11b/CD18 form Mac-1. Deletion of the CD18 gene in mice produces a significant reduction in leukocyte emigration to sites of inflammation. CD44 is involved in the interaction of neutrophils with endothelial cells and the extracellular matrix during inflammation. The binding of selectins with their carbohydrate ligands also regulates adhesion of neutrophils with endothelial cells, with P- and L-selectins moderating initial interactions and E-selectin moderating subsequent interactions. Genetic disruption of the ability of neutrophils to kill internalized bacteria also impairs normal immune function, along with genetic or acquired lack of the normal number of neutrophils (neutropenia). CD11b binding to a complement component and CD16 binding to IgG Fc contribute to phagocytosis. Inflammatory cytokines activate neutrophils and chemotactic peptides attract them to sites of infection. Inflammatory molecules that activate neutrophils include IL-1, TNF, IL-6, C-reactive protein, C3a and C5a complement anaphylatoxins, leukotrienes, PAF, and histamine. Inappropriate recruitment and activation of neutrophils and the release of reactive oxygen species can damage surrounding tissues in inflammatory conditions including arthritis and reperfusion of heart tissue following myocardial infarction.

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