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Science 20 August 1993:
Vol. 261. no. 5124, pp. 1038 - 1041
DOI: 10.1126/science.8351517

Articles

Science, Vol 261, Issue 5124, 1038-1041
Copyright © 1993 by American Association for the Advancement of Science


articles

Inhibition of an in vivo antigen-specific IgE response by antibodies to CD23

L Flores-Romo, J Shields, Y Humbert, P Graber, JP Aubry, JF Gauchat, G Ayala, B Allet, M Chavez, H Bazin, and al. et

Glaxo Institute for Molecular Biology, Geneva, Switzerland.

Immunoglobulin E (IgE) mediates many allergic responses. CD23 is a 45-kilodalton type II transmembrane glycoprotein expressed in many cell types. It is a low-affinity IgE receptor and interacts specifically with CD21, thereby modulating IgE production by B lymphocytes in vitro. In an in vivo model of an allergen-specific IgE response, administration of a rabbit polyclonal antibody to recombinant human truncated CD23 resulted in up to 90 percent inhibition of ovalbumin-specific IgE synthesis. Both Fabs and intact IgG inhibited IgE production in vitro and in vivo. Thus, CD23 participates in the regulation of IgE synthesis in vivo and so could be important in allergic disease.


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
CD23 Trimers Are Preassociated on the Cell Surface Even in the Absence of Its Ligand, IgE.
M. A. Kilmon, A. E. Shelburne, Y. Chan-Li, K. L. Holmes, and D. H. Conrad (2004)
J. Immunol. 172, 1065-1073
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Inhibition of Interleukin-4-induced Class Switch Recombination by a Human Immunoglobulin Fc{gamma}-Fc{epsilon} Chimeric Protein.
T. Yamada, D. Zhu, K. Zhang, and A. Saxon (2003)
J. Biol. Chem. 278, 32818-32824
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Regulation of IgE Production Requires Oligomerization of CD23.
M. A. Kilmon, R. Ghirlando, M.-P. Strub, R. L. Beavil, H. J. Gould, and D. H. Conrad (2001)
J. Immunol. 167, 3139-3145
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Expression of a Functional Fc{epsilon}RI on Rat Eosinophils and Macrophages.
D. Dombrowicz, B. Quatannens, J.-P. Papin, A. Capron, and M. Capron (2000)
J. Immunol. 165, 1266-1271
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CD23 Exhibits Negative Regulatory Effects on Allergic Sensitization and Airway Hyperresponsiveness.
A. HACZKU, K. TAKEDA, E. HAMELMANN, J. LOADER, A. JOETHAM, I. REDAI, C. G. IRVIN, J. J. LEE, H. KIKUTANI, D. CONRAD, et al. (2000)
Am. J. Respir. Crit. Care Med. 161, 952-960
   Abstract »    Full Text »    PDF »
CD23 and Allergic Pulmonary Inflammation: Potential Role as an Inhibitor.
M. Cernadas, G. T. De Sanctis, S. J. Krinzman, D. A. Mark, C. E. Donovan, J. A. Listman, L. Kobzik, H. Kikutani, D. C. Christiani, D. L. Perkins, et al. (1999)
Am. J. Respir. Cell Mol. Biol. 20, 1-8
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Binding of Anti-CD23 Monoclonal Antibody to the Leucine Zipper Motif of Fcepsilon RII/CD23 on B Cell Membrane Promotes Its Proteolytic Cleavage. EVIDENCE FOR AN EFFECT ON THE OLIGOMER/MONOMER EQUILIBRIUM.
O. Munoz, C. Brignone, N. Grenier-Brossette, J.-Y. Bonnefoy, and J.-L. Cousin (1998)
J. Biol. Chem. 273, 31795-31800
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Expression of IgE Heavy Chain Transcripts in the Sinus Mucosa of Atopic and Nonatopic Patients with Chronic Sinusitis.
O. Ghaffar, S. R. Durham, K. Al-Ghamdi, E. Wright, P. Small, S. Frenkiel, H. J. Gould, and Q. Hamid (1998)
Am. J. Respir. Cell Mol. Biol. 18, 706-711
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Proteolytic Cleavage of CD25, the alpha  Subunit of the Human T Cell Interleukin 2 Receptor, by Der p 1, a Major Mite Allergen with Cysteine Protease Activity.
O. Schulz, H. F. Sewell, and F. Shakib (1998)
J. Exp. Med. 187, 271-275
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CD23 deficient mice develop allergic airway hyperresponsiveness following sensitization with ovalbumin.
A Haczku, K Takeda, E Hamelmann, A Oshiba, J Loader, A Joetham, C Irvin, H Kikutani, and E. Gelfand (1997)
Am. J. Respir. Crit. Care Med. 156, 1945-1955
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Inhibition of Apoptosis in a Human Pre-B-Cell Line by CD23 Is Mediated Via a Novel Receptor.
L. J. White, B. W. Ozanne, P. Graber, J.-P. Aubry, J.-Y. Bonnefoy, and W. Cushley (1997)
Blood 90, 234-243
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Allergic airway sensitization induces T cell activation but not airway hyperresponsiveness in B cell-deficient mice.
E. Hamelmann, A. T. Vella, A. Oshiba, J. W. Kappler, P. Marrack, and E. W. Gelfand (1997)
PNAS 94, 1350-1355
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Science. ISSN 0036-8075 (print), 1095-9203 (online)