Endotoxin-free heat-shock protein 70 fails to induce APC activation

被引:0
|
作者
Bausinger, H
Lipsker, D
Ziylan, U
Manié, S
Briand, JP
Cazenave, JP
Muller, S
Haeuw, JF
Ravanat, C
de la Salle, H
Hanau, D
机构
[1] INSERM, Equipe Propre 99 08, Etab Francais Sang Alsace, F-67065 Strasbourg, France
[2] Fac Med, UMR 5641, Genet Lab, Lyon, France
[3] CNRS, Inst Biol Mol & Cellulaire, Unite Propre Rech 9021, F-67084 Strasbourg, France
[4] INSERM, Unite 311, Etab Francais Sang Alsace, F-67065 Strasbourg, France
[5] Ctr Immunol Pierre Fabre, St Julien En Genevois, France
关键词
dendritic cell; heat shock protein; lipopolysaccharide;
D O I
10.1002/1521-4141(200212)32:12<3708::AID-IMMU3708>3.0.CO;2-C
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Previous work has suggested that the peptide-carrier, heat-shock protein (hsp)70, could directly activate APC. Here we show that this ability is related to endotoxin contamination of the human rhsp70 produced in Escherichia coli. Hence, the ability of 1-3 mug/ml of rhsp70 to induce the maturation of human monocyte-derived DC is abrogated in the presence of the LPS-antagonist polymyxin B or when the rhsp70 contains less than 60 IU/mg endotoxin. Such a level of contamination of the rhsp70 is, however, sufficient - in the presence of soluble rCD14, the LPS co-receptor - to induce cytokine secretion from monocytes and DC, despite the presence of polymyxin B. However, when endotoxin contamination is below 10 IU/mg, rhsp70 does not induce cytokine secretion - even in the presence of soluble rCD14 - or activate p38 mitogen-activated protein kinase signaling pathways, thus showing that an "endotoxin free" hsp70 does not activate APC.
引用
收藏
页码:3708 / 3713
页数:6
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