Activation of the adhesive capacity of CR3 on neutrophils by endotoxin: dependence on lipopolysaccharide binding protein and CD14.

DOI PDF 被引用文献13件
  • S D Wright
    Laboratory of Cellular Physiology and Immunology, Rockefeller University, New York, New York 10021.
  • R A Ramos
    Laboratory of Cellular Physiology and Immunology, Rockefeller University, New York, New York 10021.
  • A Hermanowski-Vosatka
    Laboratory of Cellular Physiology and Immunology, Rockefeller University, New York, New York 10021.
  • P Rockwell
    Laboratory of Cellular Physiology and Immunology, Rockefeller University, New York, New York 10021.
  • P A Detmers
    Laboratory of Cellular Physiology and Immunology, Rockefeller University, New York, New York 10021.

抄録

<jats:p>Tumor necrosis factor alpha, granulocyte colony-stimulating factor, granulocyte/macrophage colony-stimulating factor, and formyl peptide were each found to cause a twofold increase in expression of CD14 on the surface of polymorphonuclear leukocytes (PMN). Upregulation of CD14 was complete by 20 min and thus appeared to result from expression of preformed stores of protein. The CD14 on the surface of PMN was shown to serve two biological functions. It bound particles coated with complexes of lipopolysaccharide (LPS) and LPS binding protein (LBP). This binding activity was enhanced by agonists that upregulated CD14 expression and may serve in the clearance of Gram-negative bacteria opsonized with LBP. Interaction of CD14 with LPS in the presence of LBP or serum also caused a dramatic, transient increase in the adhesive activity of CR3 (CD11b/CD18) on PMN. Enhanced activity of CR3 and other members of the CD11/CD18 family underlies many of the known physiological responses of PMN to LPS and may be a central feature of the in vivo responses of PMN to endotoxin.</jats:p>

収録刊行物

被引用文献 (13)*注記

もっと見る

キーワード

詳細情報 詳細情報について

問題の指摘

ページトップへ