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
Laboratory of Experimental Immunology, Faculty of Medicine, Université Libre de Bruxelles, Brussels, Belgium.
Eur J Immunol. 2002 Jan;32(1):174-81. doi: 10.1002/1521-4141(200201)32:1<174::AID-IMMU174>3.0.CO;2-L.
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.
