First published July 1, 2000 - More info
Neonatal injection of semiallogeneic spleen cells in BALB/c mice induces a self-limited state of chimerism that promotes the differentiation of donor-specific CD4 T cells toward the Th2 phenotype. Here we show that injection of spleen cells from β2-microglobulin–deficient (BALB/c × C57BL/6) F1 mice into BALB/c newborns with a disrupted β2-microglobulin (β2m) gene results in a lethal lymphoproliferative disorder associated with uncontrolled Th2 response, long-term persistence of donor B cells, and sustained blood eosinophilia. Autoimmune manifestations are also enhanced and characterized by a severe autoantibody-mediated glomerulonephritis. Histological examination of the spleen shows a hyperplasia of periarteriolar lymphoid sheaths, with accumulation of eosinophils and basophils, and variable degree of fibrosis. Perivascular lymphoid infiltrates with eosinophils are also found in the lung and are correlated with disease severity. Such abnormalities are almost absent using β2m-sufficient mice. These data demonstrate that induction of lymphoid chimerism in the absence of MHC class I–T-cell interactions results in a lethal form of host-versus-graft disease that represents a unique model of Th2-dependent chronic inflammatory disease associated with an hypereosinophilic syndrome in mice.
Jérôme D. Coudert, Gilles Foucras, Cécile Demur, Christiane Coureau, Catherine Mazerolles, Georges Delsol, Philippe Druet, Jean-Charles Guéry
J. Clin. Invest.105:1125–1132 (2000)
The authors wish to apologize for the oversight in the Acknowledgment section of their recently published paper. The correct section appears below.
We thank M. Calise, S. Pilipenko, and M. Marche for their skillful technical assistance. This work was supported by Institut National de la Santé et de la Recherche Médicale (INSERM), and grants from Conseil Général de Région Midi-Pyrénées, Etablissement Français des Greffes, and Université Paul Sabatier and Association pour la Recherche contre le Cancer. G. Foucras is on a leave of absence from Ecole Nationale Vétérinaire de Toulouse, France. J. Coudert is supported by the Ministère de l’Education Nationale, de la Recherche et de la Technologie. We thank D. Abramowicz for his helpful comments on the manuscript.