The disulfide bond between cysteine 10 and ...
Document type :
Article dans une revue scientifique: Article original
PMID :
Title :
The disulfide bond between cysteine 10 and cysteine 34 is required for CCL18 activity.
Author(s) :
Legendre, Benjamin [Auteur]
Tokarski, Caroline [Auteur]
Miniaturisation pour la Synthèse, l’Analyse et la Protéomique - UAR 3290 [MSAP]
Chang, Ying [Auteur]
de Freitas Caires, Nathalie [Auteur]
Lortat-Jacob, Hugues [Auteur]
Institut de biologie structurale [IBS - UMR 5075 ]
Nadaï, Patricia De [Auteur]
Rolando, Christian [Auteur]
Miniaturisation pour la Synthèse, l’Analyse et la Protéomique - UAR 3290 [MSAP]
Duez, Catherine [Auteur]
Biomolécules et inflammation pulmonaire
Tsicopoulos, Anne [Auteur]
Lassalle, Philippe [Auteur]
Biomolécules et inflammation pulmonaire

Tokarski, Caroline [Auteur]
Miniaturisation pour la Synthèse, l’Analyse et la Protéomique - UAR 3290 [MSAP]
Chang, Ying [Auteur]
de Freitas Caires, Nathalie [Auteur]
Lortat-Jacob, Hugues [Auteur]
Institut de biologie structurale [IBS - UMR 5075 ]
Nadaï, Patricia De [Auteur]
Rolando, Christian [Auteur]

Miniaturisation pour la Synthèse, l’Analyse et la Protéomique - UAR 3290 [MSAP]
Duez, Catherine [Auteur]
Biomolécules et inflammation pulmonaire
Tsicopoulos, Anne [Auteur]

Lassalle, Philippe [Auteur]
Biomolécules et inflammation pulmonaire
Journal title :
Cytokine
Pages :
463-70
Publisher :
Elsevier
Publication date :
2013-10
ISSN :
1043-4666
HAL domain(s) :
Sciences du Vivant [q-bio]/Biochimie, Biologie Moléculaire
English abstract : [en]
Asthma is a Th2-mediated disease that involves Th2 cell and eosinophil migration into the bronchial mucosa which is dependent upon the expression of a specific set of chemokines within the lung. Among them, CCL18 seems to ...
Show more >Asthma is a Th2-mediated disease that involves Th2 cell and eosinophil migration into the bronchial mucosa which is dependent upon the expression of a specific set of chemokines within the lung. Among them, CCL18 seems to play a key role because of its preferential expression in the lung, and its up-regulation by Th2 cytokines. Here, we show that the optimal naïve T cell and basophil chemotaxis, and basophil histamine release induced by rhCCL18 occurred at a 100 time lower concentration with CHO-derived rhCCL18 than with E. coli-derived rhCCL18. FT-ICR mass spectrometry of the intact chemokines showed that the rhCCL18 produced by CHO cells contained the 2 disulfide bonds Cys10-Cys34 and Cys11-Cys50, in clear contrast to the rhCCL18 derived from E. coli where the Cys10-Cys34 bond was absent. We found that reduction of the Cys10-Cys34 of the CHO-derived rhCCL18 resulted in a shift of its activity, reaching the same level as the E. coli-derived rhCCL18. These results demonstrate that the Cys10-Cys34 disulfide bond is involved in the function of CCL18.Show less >
Show more >Asthma is a Th2-mediated disease that involves Th2 cell and eosinophil migration into the bronchial mucosa which is dependent upon the expression of a specific set of chemokines within the lung. Among them, CCL18 seems to play a key role because of its preferential expression in the lung, and its up-regulation by Th2 cytokines. Here, we show that the optimal naïve T cell and basophil chemotaxis, and basophil histamine release induced by rhCCL18 occurred at a 100 time lower concentration with CHO-derived rhCCL18 than with E. coli-derived rhCCL18. FT-ICR mass spectrometry of the intact chemokines showed that the rhCCL18 produced by CHO cells contained the 2 disulfide bonds Cys10-Cys34 and Cys11-Cys50, in clear contrast to the rhCCL18 derived from E. coli where the Cys10-Cys34 bond was absent. We found that reduction of the Cys10-Cys34 of the CHO-derived rhCCL18 resulted in a shift of its activity, reaching the same level as the E. coli-derived rhCCL18. These results demonstrate that the Cys10-Cys34 disulfide bond is involved in the function of CCL18.Show less >
Language :
Anglais
Peer reviewed article :
Oui
Audience :
Internationale
Popular science :
Non
Source :
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