Control of In vivo IgE Production in the Mouse by Interleukin 4

  1. Derek J. Chadwick Organizer,
  2. David Evered Organizer and
  3. Julie Whelan
  1. Fred D. Finkelman1,
  2. Ildy M. Katona1,2,
  3. Joseph F. Urban Jr3 and
  4. William E. Paul4

Published Online: 28 SEP 2007

DOI: 10.1002/9780470513866.ch2

Ciba Foundation Symposium 147 - IgE, Mast Cells and the Allergic Response

Ciba Foundation Symposium 147 - IgE, Mast Cells and the Allergic Response

How to Cite

Finkelman, F. D., Katona, I. M., Urban, J. F. and Paul, W. E. (2007) Control of In vivo IgE Production in the Mouse by Interleukin 4, in Ciba Foundation Symposium 147 - IgE, Mast Cells and the Allergic Response (eds D. J. Chadwick, D. Evered and J. Whelan), John Wiley & Sons, Ltd., Chichester, UK. doi: 10.1002/9780470513866.ch2

Author Information

  1. 1

    Department of Internal Medicine, Uniformed Services University of Health Sciences, Bethesda, MD 20814-4799, USA

  2. 2

    Department of Pediatrics, Uniformed Services University of the Health Sciences, Bethesda, MD 20814

  3. 3

    Helminthic Diseases Laboratory, Agricultural Research Service, US Department of Agriculture, Beltsville, MD 20705

  4. 4

    Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA

Publication History

  1. Published Online: 28 SEP 2007

ISBN Information

Print ISBN: 9780471923091

Online ISBN: 9780470513866

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Keywords:

  • IgE production;
  • interleukin 4;
  • heligmosomoides polygyrus;
  • inoculation;
  • cytokines

Summary

In vitro studies have demonstrated that the cytokine IL-4 can, with the proper co-stimuli, induce IgE secretion. We have demonstrated in in vivo studies with a monoclonal anti-IL-4 antibody that this cytokine is required for the generation of the polyclonal primary IgE responses induced by injecting mice with GaMδ antibody or inoculating them with larvae of the nematode parasite Nippostrongylus brasiliensis (Nb), as well as for the secondary TNP-specific IgE response induced by immunizing mice with TNP-KLH on alum. We now report studies that demonstrate that: (1) the secondary polyclonal IgE response induced by repeated Nb inoculation, while mostly inhibitable by anti-IL-4 antibody, has an IL-4-independent component; (2) whereas treatment with anti-IL-4 antibody during a primary Nb inoculation does not prevent the rapid generation of a large IgE response during a second inoculation, treatment with anti-IL-4 antibody during both primary and secondary inoculation inhibits the development of a secondary IgE response by greater than 99%; (3) an established ongoing chronic IgE response, induced by inoculation of mice with larvae of the nematode parasite Heligmosomoides polygyrus (Hp), can be reduced by greater than 95% by administration of anti-IL-4 antibody; and (4) an anti-IL-4 receptor antibody effectively, efficiently and selectively blocks the GaM6 antibody-induced IgE response. These observations suggest that approaches aimed at blocking IL-4 effects may be useful for treating IgE-mediated diseases.