help button home button
AJRCCM
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by HACZKU, A.
Right arrow Articles by GELFAND, E. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by HACZKU, A.
Right arrow Articles by GELFAND, E. W.

Am. J. Respir. Crit. Care Med., Volume 156, Number 6, December 1997, 1945-1955

CD23 Deficient Mice Develop Allergic Airway Hyperresponsiveness Following Sensitization with Ovalbumin

ANGELA HACZKU, KATSUYUKI TAKEDA, ECKARD HAMELMANN, AKIHIRO OSHIBA, JOAN LOADER, ANTHONY JOETHAM, CHARLES IRVIN, HITOSHI KIKUTANI, and ERWIN W. GELFAND

Division of Basic Sciences, Department of Pediatrics and Department of Medicine, National Jewish Medical and Research Center, Denver, Colorado; and Institute for Molecular and Cellular Biology, Osaka University, Suita, Osaka, Japan

The low affinity receptor for IgE (CD23) is reported to regulate immune and inflammatory events and as a result, it may have a role in the development of allergic airway inflammation and hyperresponsiveness (AHR). To test this hypothesis CD23-deficient mice were studied following different modes of allergic sensitization. Mice were actively sensitized either intraperitoneally with ovalbumin (OA)/alum or via the airways (10 days exposure to OA aerosol with no adjuvant). Passive sensitization was performed by intravenous injections of OA-specific IgE. Airway responsiveness, serum IgE and IgG levels were assessed together with airway inflammation. Passive sensitization followed by airway challenges resulted in increased OA-specific IgG and IgE in the serum of wild-type mice only, while both the CD23+/+ and CD23-/- groups developed tracheal smooth muscle hyperresponsiveness to electrical field stimulation, indicating that IgE/CD23-mediated immune functions may not be necessary for the development of allergic changes. Active sensitization of both CD23-/- and CD23+/+ mice resulted in increased serum levels of OA-specific IgE and IgG, airway eosinophilia and significant AHR when compared with nonsensitized mice. The genetic deficiency of CD23-/- mice not only failed to prevent but was associated with a significant increase of these responses. These results indicate that CD23 may not be essential for the development of allergen-induced AHR and further, that its presence may have some inhibitory effects on the allergic response.




This article has been cited by other articles:


Home page
 J. Immunol.Home page
C. von Garnier, M. E. Wikstrom, G. Zosky, D. J. Turner, P. D. Sly, M. Smith, J. A. Thomas, S. R. Judd, D. H. Strickland, P. G. Holt, et al.
Allergic Airways Disease Develops after an Increase in Allergen Capture and Processing in the Airway Mucosa
J. Immunol., November 1, 2007; 179(9): 5748 - 5759.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
K. Kitamura, K. Takeda, T. Koya, N. Miyahara, T. Kodama, A. Dakhama, T. Takai, A. Hirano, M. Tanimoto, M. Harada, et al.
Critical Role of the Fc Receptor {gamma}-Chain on APCs in the Development of Allergen-Induced Airway Hyperresponsiveness and Inflammation
J. Immunol., January 1, 2007; 178(1): 480 - 488.
[Abstract] [Full Text] [PDF]

Home page
 CVIHome page
D. P. Ennis, J. P. Cassidy, and B. P. Mahon
Acellular Pertussis Vaccine Protects against Exacerbation of Allergic Asthma Due to Bordetella pertussis in a Murine Model
Clin. Vaccine Immunol., March 1, 2005; 12(3): 409 - 417.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
A. Wittke, V. Weaver, B. D. Mahon, A. August, and M. T. Cantorna
Vitamin D Receptor-Deficient Mice Fail to Develop Experimental Allergic Asthma
J. Immunol., September 1, 2004; 173(5): 3432 - 3436.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Cell Mol. Bio.Home page
E. M. Kudlacz, C. J. Andresen, M. Salafia, C. A. Whitney, B. Naclerio, and P. S. Changelian
Genetic Ablation of the src Kinase p59fynT Exacerbates Pulmonary Inflammation in an Allergic Mouse Model
Am. J. Respir. Cell Mol. Biol., April 1, 2001; 24(4): 469 - 474.
[Abstract] [Full Text]

Home page
 Am. J. Respir. Cell Mol. Bio.Home page
E. Hamelmann, K. Takeda, A. Haczku, G. Cieslewicz, L. Shultz, Q. Hamid, Z. Xing, J. Gauldie, and E. W. Gelfand
Interleukin (IL)-5 but Not Immunoglobulin E Reconstitutes Airway Inflammation and Airway Hyperresponsiveness in IL-4-Deficient Mice
Am. J. Respir. Cell Mol. Biol., September 1, 2000; 23(3): 327 - 334.
[Abstract] [Full Text]

Home page
 Am. J. Respir. Crit. Care Med.Home page
A. HACZKU, K. TAKEDA, E. HAMELMANN, J. LOADER, A. JOETHAM, I. REDAI, C. G. IRVIN, J. J. LEE, H. KIKUTANI, D. CONRAD, et al.
CD23 Exhibits Negative Regulatory Effects on Allergic Sensitization and Airway Hyperresponsiveness
Am. J. Respir. Crit. Care Med., March 1, 2000; 161(3): 952 - 960.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Cell Mol. Bio.Home page
E. Hamelmann, K. Takeda, J. Schwarze, A. T. Vella, C. G. Irvin, and E. W. Gelfand
Development of Eosinophilic Airway Inflammation and Airway Hyperresponsiveness Requires Interleukin-5 but Not Immunoglobulin E or B Lymphocytes
Am. J. Respir. Cell Mol. Biol., October 1, 1999; 21(4): 480 - 489.
[Abstract] [Full Text]

Home page
 Am. J. Respir. Crit. Care Med.Home page
A. TOMKINSON, A. KANEHIRO, N. RABINOVITCH, A. JOETHAM, G. CIESLEWICZ, and E. W. GELFAND
The Failure of STAT6-deficient Mice to Develop Airway Eosinophilia and Airway Hyperresponsiveness Is Overcome by Interleukin-5
Am. J. Respir. Crit. Care Med., October 1, 1999; 160(4): 1283 - 1291.
[Abstract] [Full Text]

Home page
 Am. J. Respir. Crit. Care Med.Home page
E. HAMELMANN, G. CIESLEWICZ, J. SCHWARZE, T. ISHIZUKA, A. JOETHAM, C. HEUSSER, and E. W. GELFAND
Anti-interleukin 5 But Not Anti-IgE Prevents Airway Inflammation and Airway Hyperresponsiveness
Am. J. Respir. Crit. Care Med., September 1, 1999; 160(3): 934 - 941.
[Abstract] [Full Text]

Home page
 J. Exp. Med.Home page
G. T. De Sanctis, J. A. MacLean, K. Hamada, S. Mehta, J. A. Scott, A. Jiao, C. N. Yandava, L. Kobzik, W. W. Wolyniec, A. J. Fabian, et al.
Contribution of Nitric Oxide Synthases 1, 2, and 3 to Airway Hyperresponsiveness and Inflammation in a Murine Model of Asthma
J. Exp. Med., May 17, 1999; 189(10): 1621 - 1630.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Crit. Care Med.Home page
A. HACZKU, K. TAKEDA, I. REDAI, E. HAMELMANN, G. CIESLEWICZ, A. JOETHAM, J. LOADER, J. J. LEE, C. IRVIN, and E. W. GELFAND
Anti-CD86 (B7.2) Treatment Abolishes Allergic Airway Hyperresponsiveness in Mice
Am. J. Respir. Crit. Care Med., May 1, 1999; 159(5): 1638 - 1643.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Cell Mol. Bio.Home page
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.
CD23 and Allergic Pulmonary Inflammation: Potential Role as an Inhibitor
Am. J. Respir. Cell Mol. Biol., January 1, 1999; 20(1): 1 - 8.
[Abstract] [Full Text]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Proc. Am. Thorac. Soc. Am. J. Respir. Cell Mol. Biol.
Copyright © 1997 American Thoracic Society