par Le Moine, Alain ;Flamand, Véronique ;De Lavareille, Aurore ;Paulart, Frédéric ;Buonocore, Sofia ;Vanderhaeghen, Marie-Line;Nagy, Nathalie ;Habran, Claude;Kiss, Robert ;Abramowicz, Daniel ;Goldman, Michel
Référence European Journal of Immunology, 32, 1, page (174-181)
Publication Publié, 2002-01
Référence European Journal of Immunology, 32, 1, page (174-181)
Publication Publié, 2002-01
Article révisé par les pairs
Résumé : | A significant proportion of patients with the hypereosinophilic syndrome suffer from oligoclonal expansion of type 2 helper T lymphocytes (Th2). Herein, we first provide evidence that mice immunized at birth against a single MHC class II alloantigen develop pathological features mimicking this variant of the hypereosinophilic syndrome. Indeed, C57BL / 6 mice injected at birth with (C57BL/ 6 x bm12)F1 spleen cells displayed T lymphocytes producing high levels of IL-5 and IL-13, increased blood eosinophil counts, eosinophilic infiltrates in various tissues, hyperplasia of lymphoid tissues, as well as serum hyperIgE. Moreover, eotaxin mRNA accumulated in the spleen of these animals. IL-4-deficient mice developed neither expansion of Th2 cells nor pathological changes except splenomegaly. Eotaxin mRNA accumulation was also prevented in these animals. We conclude that neonatal exposure to a single MHC class II alloantigen is sufficient to elicit an IL-4-dependent hypereosinophilic syndrome mimicking the lymphocytic variant of this disorder in humans. |