title: T cell activation, from atopy to asthma: more a paradox than a paradigm.
abstract: During the last 15 years, it was largely shown that allergic inflammation was orchestrated by activated Th2 lymphocytes, leading to IgE production and eosinophil activation. Indeed, Th2 activation was shown to be necessary to induce allergic sensitization in animal models. In humans, a Th2 skewing was shown in atopic children soon after birth. In asthma, descriptive studies showed that Th2 cells were more numerous in patients than in controls. In addition, during specific allergen stimulation, an increase of Th2 cells was described in most cases. According to this Th2 paradigm, it was proposed that early avoidance of microbial exposure could explain the increase of atopic diseases seen in the last 20 years in developed countries, as the "hygiene hypothesis". Recently, it was proposed that early exposure to lipopolysaccharide (LPS) could be protective against atopic diseases. However, it is well established that exposure to LPS can induce asthma symptoms, both in animals and humans, although it induces a Th1 inflammatory response. In addition, most infections induce asthma exacerbations and Th1 responses. Recently, some studies have showed that some Th1 cells were present in asthmatic patients, which could be related to bronchial hyperreactivity. There is therefore an "infectious paradox" in asthma, which contributes to show that the Th2 paradigm is insufficient to explain the whole inflammatory reaction of this disease. We propose that the Th2paradigm is relevant to atopy and inception of asthma albeit a Th1 activation would account at least in part for bronchial hyperreactivity and asthma symptoms.
authors.affiliation: UPRES EA 3287, Groupe de Recherche Clinique Pathologie respiratoire liée à l'environnement, Université de la Méditerranée, Service de Pneumo-Allergologie Hôpital Ste Marguerite, 270 Boulevard de Ste Marguerite, BP 29, 13274 Marseilles Cedex 09, France.
authors.forename: M
authors.initials: M
authors.lastname: El Biaze
authors.forename: S
authors.initials: S
authors.lastname: Boniface
authors.forename: V
authors.initials: V
authors.lastname: Koscher
authors.forename: E
authors.initials: E
authors.lastname: Mamessier
authors.forename: P
authors.initials: P
authors.lastname: Dupuy
authors.forename: F
authors.initials: F
authors.lastname: Milhe
authors.forename: M
authors.initials: M
authors.lastname: Ramadour
authors.forename: D
authors.initials: D
authors.lastname: Vervloet
authors.forename: A
authors.initials: A
authors.lastname: Magnan
mesh_terms: D000818:Animals; D001249:Asthma / Q000503:physiopathology*; D004195:Disease Models, Animal; D006801:Humans; D006967:Hypersensitivity / Q000503:physiopathology*; D008213:Lymphocyte Activation; D013601:T-Lymphocytes; D018417:Th1 Cells; D018418:Th2 Cells