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Belge, K.-U.* ; Dayyani, F. ; Horelt, A.* ; Siedlar, M.* ; Frankenberger, M. ; Frankenberger, B. ; Espevik, T.* ; Ziegler-Heitbrock, L.

The Proinflammatory CD14+CD16+DR++ Monocytes Are a Major Source of TNF1.

J. Immunol. 168, 3536-3542 (2002)
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
In human blood two monocyte populations can be distinguished, i.e.,, the CD14(++)CD16(-)DR(+) classical monocytes and the CD14(+)CD16(+)DR(++) proinflammatory monocytes that account for only 10% of all monocytes. We have studied TNF production in these two types of cells using three-color immunofluorescence and flow cytometry on whole peripheral blood samples stimulated with either LPS or with the bacterial lipopeptide S-(2,3-bis(palmityloxy)-(2-RS)-propyl)-N-palmitoyl-(R)-Cys-(S)-Ser-(S)-LVS4_ OH,trihydrochloride (Pam3Cys). After stimulation with LPS the median fluorescence intensity for TNF protein was 3-fold higher in the proinflammatory monocytes when compared with the classical monocytes. After stimulation with Pam3Cys they almost exclusively responded showing 10-fold-higher levels of median fluorescence intensity for TNF protein. The median fluorescence intensity, for Toll-like receptor 2 cell surface protein was found 2-fold higher on CD14(+)CD16(+)DR(++) ' monocytes, which may explain, in part, the higher Pam3Cys-induced TNF production by these cells. When analyzing secretion of TNF protein into the supernatant in PBMCs after depletion of CD16(+) monocytes we found a reduction of LPS-induced TNF by 28% but Pam3Cys-induced TNF was reduced by 64%. This indicates that the minor population of CD14+CD16+ monocytes are major producers of TNF in human blood.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter TOLL-LIKE RECEPTOR-2; CELL WALL COMPONENTS; BLOOD MONOCYTES; MEMBRANE-PROTEINS; CUTTING EDGE; LIPOPOLYSACCHARIDE; SUBPOPULATION; RESPONSIVENESS; LIPOPROTEINS; RECOGNITION
ISSN (print) / ISBN 0022-1767
e-ISSN 1550-6606
Zeitschrift Journal of Immunology
Quellenangaben Band: 168, Heft: , Seiten: 3536-3542 Artikelnummer: , Supplement: ,
Verlag American Association of Immunologists
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Molecular Immunology (IMI)
Institute of Lung Health and Immunity (LHI)