| First Author | Le Moine A | Year | 2002 |
| Journal | Eur J Immunol | Volume | 32 |
| Issue | 1 | Pages | 174-81 |
| PubMed ID | 11754358 | Mgi Jnum | J:73934 |
| Mgi Id | MGI:2157208 | Doi | 10.1002/1521-4141(200201)32:1<174::AID-IMMU174>3.0.CO;2-L |
| Citation | Le Moine A, et al. (2002) Hypereosinophilic syndrome induced by neonatal immunization against MHC class II alloantigen: critical role of IL-4. Eur J Immunol 32(1):174-81 |
| abstractText | 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. |
