Neutrophil Mac-1 and MEL-14 adhesion proteins inversely regulated by chemotactic factors.

The neutrophil Mac-1 and gp100MEL-14 adhesion proteins are involved in neutrophil extravasation during inflammation. Both the expression and activity of Mac-1 are greatly increased after neutrophil activation. In contrast, neutrophils shed gp100MEL-14 from the cell surface within 4 minutes after activation with chemotactic factors or phorbol esters, releasing a 96-kilodalton fragment of the antigen into the supernatant. Immunohistology showed that gp100MEL-14 was downregulated on neutrophils that had extravasated into inflamed tissue. The gp100MEL-14 adhesion protein may participate in the binding of unactivated neutrophils to the endothelium; rapid shedding of gp100MEL-14 may prevent extravasation into and damage of normal tissues by activated neutrophils.

[1]  C. Smith,et al.  Cooperative interactions of LFA-1 and Mac-1 with intercellular adhesion molecule-1 in facilitating adherence and transendothelial migration of human neutrophils in vitro. , 1989, The Journal of clinical investigation.

[2]  F. Luscinskas,et al.  Endothelial-leukocyte adhesion molecule-1-dependent and leukocyte (CD11/CD18)-dependent mechanisms contribute to polymorphonuclear leukocyte adhesion to cytokine-activated human vascular endothelium. , 1989, Journal of immunology.

[3]  I. Weissman,et al.  Mouse lymph node homing receptor cDNA clone encodes a glycoprotein revealing tandem interaction domains. , 1989, Science.

[4]  C W Smith,et al.  Recognition of an endothelial determinant for CD 18-dependent human neutrophil adherence and transendothelial migration. , 1988, The Journal of clinical investigation.

[5]  F. Sánchez‐Madrid,et al.  Intracellular location of T200 and Mo1 glycoproteins in human neutrophils. , 1988, The Journal of biological chemistry.

[6]  R. Winchester,et al.  Dissociation between increased surface expression of gp165/95 and homotypic neutrophil aggregation. , 1988, Journal of immunology.

[7]  L. F. Fajardo,et al.  Hyperthermia inhibits angiogenesis. , 1988, Radiation research.

[8]  J. Harlan,et al.  Increased surface expression of CD11b/CD18 (Mac-1) is not required for stimulated neutrophil adherence to cultured endothelium. , 1988, The Journal of clinical investigation.

[9]  P. J. Simpson,et al.  Reduction of experimental canine myocardial reperfusion injury by a monoclonal antibody (anti-Mo1, anti-CD11b) that inhibits leukocyte adhesion. , 1988, The Journal of clinical investigation.

[10]  G. Zimmerman,et al.  Neutrophil adherence to human endothelium in vitro occurs by CDw18 (Mo1, MAC-1/LFA-1/GP 150,95) glycoprotein-dependent and -independent mechanisms. , 1988, The Journal of clinical investigation.

[11]  H. Rosen,et al.  Monoclonal antibody to the murine type 3 complement receptor inhibits adhesion of myelomonocytic cells in vitro and inflammatory cell recruitment in vivo , 1987, The Journal of experimental medicine.

[12]  T. Springer,et al.  Stimulated mobilization of monocyte Mac-1 and p150,95 adhesion proteins from an intracellular vesicular compartment to the cell surface. , 1987, The Journal of clinical investigation.

[13]  E. Butcher,et al.  Leukocyte-endothelial cell recognition: evidence of a common molecular mechanism shared by neutrophils, lymphocytes, and other leukocytes. , 1987, Journal of immunology.

[14]  E. Butcher,et al.  Receptors involved in lymphocyte homing: relationship between a carbohydrate-binding receptor and the MEL-14 antigen , 1987, The Journal of cell biology.

[15]  S. Wright,et al.  Phorbol esters cause sequential activation and deactivation of complement receptors on polymorphonuclear leukocytes. , 1986, Journal of immunology.

[16]  T. Yednock,et al.  Involvement of sialic acid on endothelial cells in organ-specific lymphocyte recirculation. , 1985, Science.

[17]  T. Springer,et al.  Inherited deficiency of the Mac-1, LFA-1, p150,95 glycoprotein family and its molecular basis , 1984, The Journal of experimental medicine.

[18]  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.

[19]  M. Gimbrone,et al.  Studies on the interaction between GP-18-0-deficient neutrophils and vascular endothelium. , 1982, Blood.

[20]  L. Herzenberg,et al.  Xenogeneic Monoclonal Antibodies to Mouse Lymphoid Differentiation Antigens * , 1979, Immunological reviews.

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

[22]  Michael Loran Dustin,et al.  The leukocyte integrins. , 1989, Advances in immunology.

[23]  L. Lindbom,et al.  A monoclonal antibody to the membrane glycoprotein complex CD18 inhibits polymorphonuclear leukocyte accumulation and plasma leakage in vivo , 1987 .

[24]  T. Springer,et al.  Leukocyte adhesion deficiency: an inherited defect in the Mac-1, LFA-1, and p150,95 glycoproteins. , 1987, Annual review of medicine.

[25]  C. Parker.  Lipid mediators produced through the lipoxygenase pathway. , 1987, Annual Review of Immunology.

[26]  S. Jalkanen,et al.  A lymphoid cell surface glycoprotein involved in endothelial cell recognition and lymphocyte homing in man , 1986, European journal of immunology.