Hyper immunoglobulin E response in mice with monoclonal populations of B and T lymphocytes

Maria A. Curotto De Lafaille, Stephanie Muriglan, Mary Jean Sunshine, Ying Lei, Nino Kutchukhidze, Gláucia C. Furtado, Allen K. Wensky, Danyvid Olivares-Villagómez, Juan J. Lafaille

Research output: Contribution to journalArticlepeer-review

100 Scopus citations


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 α/β 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.

Original languageEnglish
Pages (from-to)1349-1359
Number of pages11
JournalJournal of Experimental Medicine
Issue number9
StatePublished - 2001
Externally publishedYes


  • Atopy
  • Immunoglobulin class switching
  • Mice
  • Mutant strains
  • T lymphocytes, regulatory
  • Th2 differentiation


Dive into the research topics of 'Hyper immunoglobulin E response in mice with monoclonal populations of B and T lymphocytes'. Together they form a unique fingerprint.

Cite this