The Journal of Experimental Medicine
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Published 5 November 2001. doi:10.1084/jem.194.9.1349
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© Rockefeller University Press, 0022-1007/2001/11/1349/ $5.00
The Journal of Experimental Medicine, Volume 194, Number 9, November 5, 2001 1349-1360

Original Article

 Hyper Immunoglobulin E Response in Mice with Monoclonal Populations of B and T Lymphocytes1

Maria A. Curotto de Lafaille1, Stephanie Muriglan1, Mary-Jean Sunshine1, Ying Lei1, Nino Kutchukhidze1, Gláucia C. Furtado1, Allen K. Wensky1, Danyvid Olivares-Villagómez1 and Juan J. Lafaille1,2

1 Program of Molecular Pathogenesis, Skirball Institute for Biomolecular Medicine
2 Department of Pathology, New York University School of Medicine, New York, NY 10016

Address correspondence to Juan J. Lafaille, Skirball Institute of Biomolecular Medicine, 540 First Ave., New York, NY 10016. Phone: 212-263-1489; Fax: 212-263-5711; E-mail: lafaille{at}saturn.med.nyu.edu

A key event in the pathogenesis of allergies is the production of antibodies of the immunoglobulin (Ig)E class. In normal individuals the levels of IgE are tightly regulated, as illustrated by the low serum IgE concentration. In addition, multiple immunizations are usually required to generate detectable IgE responses in normal experimental animals. To define the parameters that regulate IgE production in vivo, we generated mice bearing monoclonal populations of B and T lymphocytes specific for influenza virus hemagglutinin (HA) and chicken ovalbumin (OVA), respectively. A single immunization of the monoclonal mice with the cross-linked OVA-HA antigen led to serum IgE levels that reached 30–200 µg/ml. This unusually high IgE response was prevented by the infusion of regulatory {alpha}/ß CD4+ T cells belonging to both CD25+ and CD25- subpopulations. The regulation by the infused T cells impeded the development of fully competent OVA-specific effector/memory Th2 lymphocytes without inhibiting the initial proliferative response of T cells or promoting activation-induced cell death. Our results indicate that hyper IgE responses do not occur in normal individuals due to the presence of regulatory T cells, and imply that the induction of regulatory CD4+ T cells could be used for the prevention of atopy.

Key Words: atopy • Th2 differentiation • immunoglobulin class switching • T lymphocytes, regulatory • mice, mutant strains


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