and Increased Plasma Membrane Expression of the Glycoprotein

Mol , a glycoprotein heterodimer (gp 1 55,95) that functions as an adhesion promoting molecule and as the C3bi receptor of human myeloid cells, is expressed in increased amounts in the plasma membrane after exposure of polymorphonuclear leukocytes (PMNs) to various stimuli. Previous studies have suggested that secondary granules represent an intracellular pool of Mol that, upon degranulation, fuse with the plasma membrane resulting in a tenfold increase in surface expression of Mel . To determine the intracellular location of Mel , we monitored Mel expression by immunofluorescence and compared it to the release of myeloperoxidase (MPO. a marker for the primary granules), vitamin B12 binding protein (B12BP, secondary granules), and gelatinase (gelatinase-containing organelles) following exposure to various stimuli. Human neutrophils stimulated with 20 mmol/L fluoride for 16

[1]  Edda Klipp,et al.  Biochemical network models simplified by balanced truncation , 2005, The FEBS journal.

[2]  J. Metcalf,et al.  Evidence for distinct intracellular pools of receptors for C3b and C3bi in human neutrophils. , 1985, Journal of immunology.

[3]  H. Colten,et al.  Increased expression of an adhesion-promoting surface glycoprotein in the granulocytopenia of hemodialysis. , 1985, The New England journal of medicine.

[4]  A. Kang,et al.  Secretion of collagenolytic enzymes by human polymorphonuclear leukocytes. , 1984, Collagen and related research.

[5]  Berger,et al.  Human neutrophils increase expression of C3bi as well as C3b receptors upon activation. , 1984, The Journal of clinical investigation.

[6]  M. Arnaout,et al.  Subcellular localization of the large subunit of Mo1 (Mo1 alpha; formerly gp 110), a surface glycoprotein associated with neutrophil adhesion. , 1984, The Journal of clinical investigation.

[7]  M. Arnaout,et al.  Deficiency of a leukocyte surface glycoprotein (LFA-1) in two patients with Mo1 deficiency. Effects of cell activation on Mo1/LFA-1 surface expression in normal and deficient leukocytes. , 1984, The Journal of clinical investigation.

[8]  S. Meuer,et al.  A monoclonal antibody that blocks class II histocompatibility-related immune interactions. , 1984, Human immunology.

[9]  H. Colten,et al.  Inhibition of phagocytosis of complement C3- or immunoglobulin G-coated particles and of C3bi binding by monoclonal antibodies to a monocyte-granulocyte membrane glycoprotein (Mol). , 1983, The Journal of clinical investigation.

[10]  R. Schreiber,et al.  Anti-Mac-1 selectively inhibits the mouse and human type three complement receptor , 1982, The Journal of experimental medicine.

[11]  B. Dewald,et al.  Release of gelatinase from a novel secretory compartment of human neutrophils. , 1982, The Journal of clinical investigation.

[12]  M. Baggiolini,et al.  Partial purification of collagenase and gelatinase from human polymorphonuclear leucocytes. Analysis of their actions on soluble and insoluble collagens. , 1982, The Biochemical journal.

[13]  M. L. Karnovsky,et al.  cis-Polyunsaturated fatty acids induce high levels of superoxide production by human neutrophils. , 1981, The Journal of biological chemistry.

[14]  M. Baggiolini,et al.  The latent collagenase and gelatinase of human polymorphonuclear neutrophil leucocytes. , 1980, The Biochemical journal.

[15]  E. Reinherz,et al.  A monoclonal antibody reactive with human peripheral blood monocytes. , 1980, Journal of immunology.

[16]  A. Kay,et al.  Leucoattractants enhance complement receptors on human phagocytic cells. , 1979, Clinical and experimental immunology.

[17]  J. Oliver,et al.  Superoxide production induced in rabbit polymorphonuclear leukocytes by synthetic chemotactic peptides and A23187. , 1979, The American journal of pathology.

[18]  G. Galfré,et al.  Mac‐1: a macrophage differentiation antigen identified by monoclonal antibody , 1979, European journal of immunology.

[19]  M. L. Karnovsky,et al.  Fluoride-mediated activation of the respiratory burst in human neutrophils. A reversible process. , 1979, The Journal of clinical investigation.

[20]  M. Baggiolini,et al.  Collagenase is a component of the specific granules of human neutrophil leucocytes. , 1977, The Biochemical journal.

[21]  B. Babior,et al.  Biological defense mechanisms. The effect of bacteria and serum on superoxide production by granulocytes. , 1974, The Journal of clinical investigation.

[22]  L. Wasserman,et al.  RAPID CHARCOAL ASSAY FOR INTRINSIC FACTOR (IF), GASTRIC JUICE UNSATURATED B12 BINDING CAPACITY, ANTIBODY TO IF, AND SERUM UNSATURATED B12 BINDING CAPACITY. , 1965, Blood.

[23]  B. Vallee,et al.  Metalloenzymes and myocardial infarction. II. Malic and lactic dehydrogenase activities and zinc concentrations in serum. , 1956, The New England journal of medicine.

[24]  R. Dulbecco,et al.  PLAQUE FORMATION AND ISOLATION OF PURE LINES WITH POLIOMYELITIS VIRUSES , 1954, The Journal of experimental medicine.

[25]  K A Muirhead,et al.  Determination of linear fluorescence intensities from flow cytometric data accumulated with logarithmic amplifiers. , 1983, Cytometry.

[26]  C. Terhorst,et al.  Structural analysis of differentiation antigens Mo1 and Mo2 on human monocytes. , 1982, Hybridoma.

[27]  Kyoko,et al.  Identification of the C 3 bi receptor of human monocytes and macrophages by using monoclonal antibodies ( phagocytosis / complement / OKM 1 ) , 2022 .