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Involvement of CCL18 in Allergic Asthma¹

Patricia de Nadaï^*, Anne-Sophie Charbonnier^*, Cécile Chenivesse^*, Stéphanie Sénéchal^*, Clément Fournier, Jules Gilet^*, Han Vorng^*, Ying Chang^*,, Philippe Gosset^*, Benoît Wallaert^*,, André-Bernard Tonnel^*,, Philippe Lassalle^* and Anne Tsicopoulos^2,*,

^* Institut National de la Sante et de la Recherche Medicale U-774, Institut Pasteur de Lille, Lille, France; Clinique des Maladies Respiratoires et Centre Hospitalier Régional et Universitaire de Lille, Lille, France; and Department of Central Research, the Third Clinical College, Jilin University, Jilin, China

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.

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