Mechanism Regulating Recruitment of CD11b/CD18 to the Cell Surface is Distinct From That Which Induces Adhesion in Homotypic Neutrophil Aggregation
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).
KeywordsPhorbol Myristate Acetate Phorbol Myristate Acetate Sodium Salicylate Neutrophil Aggregation Beta Chain
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