Article Dans Une Revue Journal of Allergy and Clinical Immunology Année : 2006

Diesel exhaust exposure favors TH2 cell recruitment in nonatopic subjects by differentially regulating chemokine production

Ying Chang
  • Fonction : Auteur
Stéphanie Sénéchal
  • Fonction : Auteur
Patricia de Nadai
  • Fonction : Auteur
Cécile Chenivesse
  • Fonction : Auteur
Jules Gilet
  • Fonction : Auteur
Han Vorng
  • Fonction : Auteur
Benjamin Legendre
André-Bernard Tonnel
  • Fonction : Auteur
Benoît Wallaert
  • Fonction : Auteur
Philippe Lassalle
  • Fonction : Auteur
Anne Tsicopoulos
  • Fonction : Auteur

Résumé

Abstract Allergic asthma is associated with a pulmonary recruitment of Th type 2 cells, basophils, and eosinophils, mainly linked to chemokine production. CCL18 is a chemokine preferentially expressed in the lung, secreted by APCs, induced by Th2-type cytokines, and only present in humans. Therefore, CCL18 may be involved in allergic asthma. PBMC from asthmatics allergic to house dust mite cultured in the presence of Dermatophagoides pteronyssinus 1 (Der p 1) allergen secreted CCL18, 48 and 72 h after stimulation, whereas those from healthy donors did not. Part of CCL18 was directly derived from Der p 1-stimulated plasmacytoid dendritic cells, whereas the other part was linked to monocyte activation by IL-4 and IL-13 produced by Der p 1-stimulated T cells. In bronchoalveolar lavages from untreated asthmatic allergic patients, CCL18 was highly increased compared with controls. Functionally, CCL18 preferentially attracted in vitro-polarized Th2 cells and basophils, but not eosinophils and Th1 cells, and induced basophil histamine and intracellular calcium release. These data show a new function for CCL18, i.e., the recruitment of Th2 cells and basophils, and suggest that CCL18 may play a predominant role in allergic asthma.

Dates et versions

hal-04462613 , version 1 (16-02-2024)

Identifiants

Citer

Ying Chang, Stéphanie Sénéchal, Patricia de Nadai, Cécile Chenivesse, Jules Gilet, et al.. Diesel exhaust exposure favors TH2 cell recruitment in nonatopic subjects by differentially regulating chemokine production. Journal of Allergy and Clinical Immunology, 2006, 118 (2), pp.354-360. ⟨10.1016/j.jaci.2006.04.050⟩. ⟨hal-04462613⟩
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