Cross-linking of sialophorin (CD43) induces neutrophil aggregation in a CD18-dependent and a CD18-independent way

Normal human neutrophils bound an as yet unclustered mAb designated BS-1. The Ag immunoprecipitated with BS-1 was blotted by CD43 mAb (and vice versa), and is therefore identical to the large sialoglycoprotein. The CD43 Ag expression on the neutrophil surface is decreased upon neutrophil activation...

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Bibliographic Details
Published in:The Journal of immunology (1950) Vol. 149; no. 3; pp. 998 - 1003
Main Authors: Kuijpers, TW, Hoogerwerf, M, Kuijpers, KC, Schwartz, BR, Harlan, JM
Format: Journal Article
Language:English
Published: Bethesda, MD Am Assoc Immnol 01-08-1992
American Association of Immunologists
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Summary:Normal human neutrophils bound an as yet unclustered mAb designated BS-1. The Ag immunoprecipitated with BS-1 was blotted by CD43 mAb (and vice versa), and is therefore identical to the large sialoglycoprotein. The CD43 Ag expression on the neutrophil surface is decreased upon neutrophil activation with the chemoattractant FMLP or with PMA. This can be (at least partially) explained by the release of CD43+ material with an altered electrophoretic mobility into the extracellular medium of the neutrophils upon activation. Cross-linking of the CD43 Ag with BS-1 also invoked neutrophil activation by itself: F(ab)2 fragments of BS-1-induced neutrophil aggregation, in contrast to F(ab) fragments. Neither respiratory burst activity nor a significant rise in intracellular Ca2+ level or actin polymerization were observed. The transient neutrophil aggregation response was largely CD18 dependent, especially in the initial phase of homotypic clustering. However, a significant CD18-independent mechanism contributed thereafter to the neutrophil aggregation, as was further substantiated by the use of cultured T (and EBV-transformed B) cell clones of a patient with a leukocyte adhesion deficiency. CD43 is the first molecule described on neutrophils able to induce adhesive properties in a dual fashion.
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ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.149.3.998