Preferred Label : Neutrophil Surface Molecule Pathway;
NCIt related terms : Neutrophil and Its Surface Molecules;
Alternative definition : BIOCARTA: 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. (This definition may be outdated - see the DesignNote.);
NCIt note : The BIOCARTA Definition (ALT_DEFINITION) for this pathway concept was provided by
BioCarta. This property was not created by, nor is it maintained by the NCI Thesaurus
staff. Additionally, BioCarta is no longer updating its pathway data; thus, the BIOCARTA
Definition might be outdated or inaccurate. Please see the Terms and Conditions for
Use at http://www.biocarta.com/.;
Biocarta ID : h_neutrophilPathway;
Origin ID : C91311;
UMLS CUI : C2984152;
Semantic type(s)
- has_gene_product_element
- pathway_has_gene_element
