Mechanism Regulating Recruitment of CD11b/CD18 to the Cell Surface is Distinct From That Which Induces Adhesion in Homotypic Neutrophil Aggregation

  • Jill P. Buyon
  • Mark R. Philips
  • Steven B. Abramson
  • Seth G. Slade
  • Gerald Weissmann
  • Robert Winchester
Conference paper

Abstract

In response to activation by certain stimuli, neutrophils undergo changes in surface properties that result in their formation of specific cellular aggregates (1). This phenomenon is being intensively studied as a model of induced homotypic cell-to-cell interaction. Evidence that heterodimeric glycoproteins of the Leu-CAM family are involved in mediating neutrophil aggregation rests on several findings; (i) most monoclonal antibodies (MAb) to CD18, the common 95 kD beta subunit (β2) abolish neutrophil aggregation (2); (ii) several of the MAb to CD11b, the 165 kD alpha subunit (also referred to as αM, CR3, or MAC-1 inhibit this response (2,3); and (iii) neutrophils from individuals genetically deficient in these molecules cannot be stimulated to aggregate (4).

Keywords

Superoxide Integrin HEPES Dition Fluorescein 

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Copyright information

© Springer-Verlag New York Inc. 1990

Authors and Affiliations

  • Jill P. Buyon
  • Mark R. Philips
  • Steven B. Abramson
  • Seth G. Slade
  • Gerald Weissmann
  • Robert Winchester

There are no affiliations available

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