Cytokine-mediated Bax deficiency and consequent delayed neutrophil apoptosis: A general mechanism to accumulate effector cells in inflammation

Proceedings of the National Academy of Sciences of the United States of America

Volumn 96, Issue 23, 1999, Pages 13330-13335

  Dibbert, Birgit ^a   Weber, Martina ^a   Nikolaizik, Wilfried H ^b   Vogt, Peter ^a   Schöni, Martin H ^c   Blaser, Kurt ^a   Simon, Hans Uwe ^a  

^a UNIVERSITY OF ZURICH   (Switzerland)

^b Alpine Children's Hospital Davos   (Switzerland)

^c UNIVERSITY OF BERN   (Switzerland)

Author keywords

[No Author keywords available]

Indexed keywords

ALPHA INTERFERON; ANTISENSE OLIGODEOXYNUCLEOTIDE; CYTOKINE; GRANULOCYTE COLONY STIMULATING FACTOR; GRANULOCYTE MACROPHAGE COLONY STIMULATING FACTOR; INTERLEUKIN 3; PROTEIN BAX; PROTEIN BCL 2; PROTEIN BCL X;

APOPTOSIS; ARTICLE; CELL SURVIVAL; CELLULAR IMMUNITY; CONTROLLED STUDY; CYSTIC FIBROSIS; FLOW CYTOMETRY; HUMAN; HUMAN CELL; HUMAN TISSUE; INFLAMMATORY DISEASE; NEUTROPHIL; NEUTROPHILIA; PRIORITY JOURNAL; PROTEIN EXPRESSION;

APOPTOSIS; BASE SEQUENCE; BCL-2-ASSOCIATED X PROTEIN; CELLS, CULTURED; CYTOKINES; DNA PRIMERS; GRANULOCYTE COLONY-STIMULATING FACTOR; GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR; HUMANS; INFLAMMATION; NEUTROPHILS; PROTO-ONCOGENE PROTEINS; PROTO-ONCOGENE PROTEINS C-BCL-2; RNA, MESSENGER;

EID: 0033539507     PISSN: 00278424     EISSN: None     Source Type: Journal    
DOI: 10.1073/pnas.96.23.13330     Document Type: Article

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