Hypereosinophilic syndrome induced by neonatal immunization against MHC class II alloantigen: critical role of IL‐4

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 varia...

Full description

Saved in:
Bibliographic Details
Published in:European journal of immunology 2002-01, Vol.32 (1), p.174-181
Main Authors: 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
Format: Article
Language:English
Subjects:
Animals
Animals, Newborn
Cytotoxicity, Immunologic - immunology
Disease Models, Animal
Eosinophil
Eotaxin
Histocompatibility Antigens Class II - immunology
Hypereosinophila
Hypereosinophilic Syndrome - immunology
IL‐4
Immunization
Interleukin-13 - immunology
Interleukin-13 - secretion
Interleukin-4 - genetics
Interleukin-4 - immunology
Interleukin-5 - immunology
Interleukin-5 - secretion
Isoantigens - immunology
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Knockout
Spleen - cytology
Spleen - immunology
T-Lymphocytes - immunology
Th2
Citations: Items that this one cites
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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 × 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.
ISSN:0014-2980
1521-4141
DOI:10.1002/1521-4141(200201)32:1<174::AID-IMMU174>3.0.CO;2-L