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Aberrant activation and regulation of the oxidative burst in neutrophils with Mo1 glycoprotein deficiency

Journal Article · · J. Immunol.; (United States)
OSTI ID:5448418
Patients whose cells are deficient in the glycoproteins LFA-1, Mo1, and p150,95 have recurrent infections and pronounced abnormalities in neutrophil adherence, aggregation, chemotaxis, and phagocytosis. Activation and regulation of oxidative metabolism of Mo1-deficient neutrophils have been characterized. These cells failed to depolarize or to produce O/sub 2//sup -/ or H/sub 2/O/sub 2/ normally when stimulated by opsonized zymosan. The chemotactic peptide formyl methionyl-leucyl-phenylalanine depolarized Mo1-deficient neutrophils normally but caused supernormal production of O/sub 2//sup -/ and H/sub 2/O/sub 2/, a result of a prolonged burst in oxidative metabolism. Phorbol myristate acetate depolarized Mo1-deficient neutrophils at a nearly normal rate but evoked release of significantly less O/sub 2//sup -/ and H/sub 2/O/sub 2/ than from normal PMN. The aberrant activation and regulation of the oxidative burst in Mo1-deficient neutrohpils are considered in light of recently 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.
Research Organization:
Univ. of Iowa, Iowa City
OSTI ID:
5448418
Journal Information:
J. Immunol.; (United States), Journal Name: J. Immunol.; (United States) Vol. 137:2; ISSN JOIMA
Country of Publication:
United States
Language:
English