Aberrant activation and regulation of the oxidative burst in neutrophils with Mol glycoprotein deficiency

W. M. Nauseef, P. De Alarcon, J. F. Bale, R. A. Clark

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Abstract

Patients whose cells are deficient in the glycoproteins LFA-1, Mol, and p150,95 have recurrent infections and pronounced abnormalities in neutrophil adherence, aggregation, chemotaxis, and phagocytosis. We characterized activation and regulation of oxidative metabolism of Mol-deficient neutrophils. These cells failed to depolarize or to produce O2- or H2O2 normally when stimulated by opsonized zymosan. The chemotactic peptide formyl methionylleucyl-phenylalanine depolarized Mol-deficient neutrophils normally but caused supernormal production of O2- and H2O2, a result of a prolonged burst in oxidative metabolism. Phorbol myristate acetate depolarized Mol-deficient neutrophils at a nearly normal rate but evoked release of significantly less O2- and H2O2 than from normal PMN. The aberrant activation and regulation of the oxidative burst in Mol-deficient neutrophils are considered in light of recently emerging concepts in the cell biology of this process, and the possibility that these abnormalities reflect a defect in the cytoskeleton-membrane interaction is discussed.

Original languageEnglish (US)
Pages (from-to)636-642
Number of pages7
JournalJournal of Immunology
Volume137
Issue number2
StatePublished - Jan 1 1986

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ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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