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This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Ottonello, L. Articles by Dallegri, F. Search for Related Content PubMed PubMed Citation Articles by Ottonello, L. Articles by Dallegri, F. Related Collections Phagocytes Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, Vol. 93 No. 10 (May 15), 1999: pp. 3505-3511 Monoclonal Lym-1 Antibody-Dependent Cytolysis by Neutrophils Exposed to Granulocyte-Macrophage Colony-Stimulating Factor: Intervention of FcRII (CD32), CD11b-CD18 Integrins, and CD66b Glycoproteins L. Ottonello, A.L. Epstein, P. Dapino, P. Barbera, P. Morone, and F. Dallegri From the Department of Internal Medicine, University of Genova Medical School, Genova, Italy; and the Department of Pathology, University of Southern California, Los Angeles, CA. Murine monoclonal antibody (MoAb) Lym-1 is an IgG2a able to bind HLA-DR variants on malignant B cells and suitable for serotherapeutic approaches in B-lymphoma patients. We have previously shown that Lym-1 can synergize with granulocyte-macrophage colony-stimulating factor (GM-CSF) to trigger neutrophil cytolysis towards Raji cells used as a model of B-lymphoma targets. Here we provide evidence for the intervention of certain neutrophil receptors or surface molecules in this model of cell-mediated lysis. The lysis was completely inhibited by the anti-FcRII MoAb IV.3 and unaffected by the anti-FcRIII MoAb 3G8. This suggests that neutrophil cytolysis involves FcRII without cooperation of this receptor with FcRIII. Moreover, the lysis was inhibited by an anti-CD18 MoAb (MEM48) and by a MoAb specific for carcinoembryonic antigen (CEA)-like and glycophosphatidyl inositol (GPI)-linked glycoproteins (CD66b). Using an immunofluorescence staining procedure, cross-linking of CD66b induced the redistribution of CD11b on neutrophils with distinct areas of CD11b clustering via a process susceptible of inhibition by D-mannose. This is consistent with the ability of CD11b-CD18 and CD66b to undergo lectin-like physical interactions on the neutrophil surface. Such a type of interaction is presumably instrumental for neutrophil cytolytic activity in that the lysis was inhibited by D-mannose and enhanced by the MoAb VIM-12, which mimics the cooperation between CD11b and GPI-anchored molecules by specifically interacting with CD11b lectin-like sites. Therefore, the present results prove the absolute requirement for FcRII in neutrophil GM-CSF/Lym-1-mediated cytolysis and, on the other hand, define the crucial role of CD66b and CD11b/CD18 in the expression of the cell lytic potential. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: L. Ottonello, A. L. Epstein, M. Mancini, P. Dapino, and F. Dallegri Monoclonal LYM-1 antibody-dependent cytolysis by human neutrophils exposed to GM-CSF: auto-regulation of target cell attack by cathepsin G J. Leukoc. Biol., January 1, 2004; 75(1): 99 - 105. [Abstract] [Full Text] [PDF] M. Ghio, L. Ottonello, P. Contini, M. Amelotti, C. Mazzei, F. Indiveri, F. Puppo, and F. Dallegri Transforming growth factor-{beta}1 in supernatants from stored red blood cells inhibits neutrophil locomotion Blood, August 1, 2003; 102(3): 1100 - 1107. [Abstract] [Full Text] [PDF] A. B. van Spriel, H. H. van Ojik, A. Bakker, M. J. H. Jansen, and J. G. J. van de Winkel Mac-1 (CD11b/CD18) is crucial for effective Fc receptor-mediated immunity to melanoma Blood, January 1, 2003; 101(1): 253 - 258. [Abstract] [Full Text] [PDF] L. Ottonello, G. Frumento, N. Arduino, M. Bertolotto, P. Dapino, M. Mancini, and F. Dallegri Differential regulation of spontaneous and immune complex-induced neutrophil apoptosis by proinflammatory cytokines. Role of oxidants, Bax and caspase-3 J. Leukoc. Biol., July 1, 2002; 72(1): 125 - 132. [Abstract] [Full Text] [PDF] L. S. Metelitsa, S. D. Gillies, M. Super, H. Shimada, C. P. Reynolds, and R. C. Seeger Antidisialoganglioside/granulocyte macrophage-colony-stimulating factor fusion protein facilitates neutrophil antibody-dependent cellular cytotoxicity and depends on Fcgamma RII (CD32) and Mac-1 (CD11b/CD18) for enhanced effector cell adhesion and azurophil granule exocytosis Blood, May 13, 2002; 99(11): 4166 - 4173. [Abstract] [Full Text] [PDF] M. Kuroki, H. Abe, T. Imakiirei, S. Liao, H. Uchida, Y. Yamauchi, S. Oikawa, and M. Kuroki Identification and comparison of residues critical for cell-adhesion activities of two neutrophil CD66 antigens, CEACAM6 and CEACAM8 J. Leukoc. Biol., October 1, 2001; 70(4): 543 - 550. [Abstract] [Full Text] [PDF] A. B. van Spriel, J. H. W. Leusen, M. van Egmond, H. B. P. M. Dijkman, K. J. M. Assmann, T. N. Mayadas, and J. G. J. van de Winkel Mac-1 (CD11b/CD18) is essential for Fc receptor-mediated neutrophil cytotoxicity and immunologic synapse formation Blood, April 15, 2001; 97(8): 2478 - 2486. [Abstract] [Full Text] [PDF] L. Ottonello, A. L. Epstein, M. Mancini, M. Amelotti, P. Dapino, and F. Dallegri Monoclonal Lym-1 antibody-targeted lysis of B lymphoma cells by neutrophils. Evidence for two mechanisms of Fc{gamma}RII-dependent cytolysis J. Leukoc. Biol., November 1, 2000; 68(5): 662 - 668. [Abstract] [Full Text]

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