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

Chang, Ying; Sénéchal, Stéphanie; De Nadai, Patricia; Chenivesse, Cécile; Gilet, Jules; Vorng, Han; Legendre, Benjamin; Tonnel, André-Bernard; Wallaert, Benoît; Lassalle, Philippe; Tsicopoulos, Anne

doi:doi/10.1016/j.jaci.2006.04.050

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

par Chang, Ying ;Sénéchal, Stéphanie ;De Nadai, Patricia

;Chenivesse, Cécile ;Gilet, Jules ;Vorng, Han ;Legendre, Benjamin ;Tonnel, André-Bernard ;Wallaert, Benoît ;Lassalle, Philippe ;Tsicopoulos, Anne
Référence Journal of allergy and clinical immunology, 118, 2, page (354-360)
Publication Publié, 2006-08

Article révisé par les pairs

Résumé :

The prevalence of allergic diseases has increased in the last 20 years, and a number of studies have shown that diesel exhaust particle-associated polyaromatic hydrocarbons can exacerbate the allergic reaction. Much less is known about their potential capacity to generate a T(H)2-type allergic reaction in nonatopic subjects.

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