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 arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Erb, K. J.
Right arrow Articles by Serfling, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Erb, K. J.
Right arrow Articles by Serfling, E.

 Previous Article  |  Next Article 

Infection and Immunity, November 2003, p. 6641-6647, Vol. 71, No. 11
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.11.6641-6647.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Mice Deficient in Nuclear Factor of Activated T-Cell Transcription Factor c2 Mount Increased Th2 Responses after Infection with Nippostrongylus brasiliensis and Decreased Th1 Responses after Mycobacterial Infection

Klaus J. Erb,1* Thomas Twardzik,2 Alois Palmetshofer,2 Gisela Wohlleben,1 Ursula Tatsch,1 and Edgar Serfling2*

Research Center for Infectious Diseases,1 Department of Molecular Pathology, Institute of Pathology, University of Wuerzburg, D-97080 Wuerzburg, Germany2

Received 27 January 2003/ Returned for modification 1 April 2003/ Accepted 4 August 2003

Infection of nuclear factor of activated T-cell transcription factor c2 (NFATc2)-deficient mice with the helminth Nippostrongylus brasiliensis led to a distinct increase in interleukin-4 (IL-4) and IL-5 protein synthesis by lymph node and spleen cells and to elevated serum immunoglobulin E (IgE) levels in comparison to those seen with infected control mice. While IL-4, IL-5, and IL-13 mRNA expression was also enhanced in lymph node cells from the lungs of infected NFATc2-/- mice, the number of T cells secreting Th2-type lymphokines remained the same in mice infected with N. brasiliensis. In contrast, lymphocytes from NFATc2-deficient mice infected with Mycobacterium bovis BCG secreted less gamma interferon than lymphocytes from infected control mice. These findings indicate that NFATc2 is an activator of Th1 responses and a suppressor of Th2 responses in vivo.

* Corresponding author. Mailing address for K. J. Erb: Research Center for Infectious Diseases, Roentgenring 11, D-97070 Wuerzburg, Germany. Phone: 49 931 31 21 74. Fax: 49-931 31 25 78. E-mail: klaus.erb{at}mail.uni-wuerzburg.de Mailing address for E. Serfling: Department of Molecular Pathology, Institute of Pathology, Josef-Schneider-Str. 2, D-97080 Wuerzburg, Germany. Phone: 49 931 201 474 31. Fax: 49 931 201 471 31. E-mail: path015{at}mail.uni-wuerzburg.de.

Editor: J. M. Mansfield

Infection and Immunity, November 2003, p. 6641-6647, Vol. 71, No. 11
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.11.6641-6647.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Becker, M., Heib, V., Klein, M., Doener, F., Bopp, T., Taube, C., Radsak, M., Schild, H., Schmitt, E., Stassen, M. (2009). Impaired Mast Cell-Driven Immune Responses in Mice Lacking the Transcription Factor NFATc2. J. Immunol. 182: 6136-6142 [Abstract] [Full Text]  
  • Kaminuma, O., Kitamura, F., Kitamura, N., Hiroi, T., Miyoshi, H., Miyawaki, A., Miyatake, S. (2008). Differential Contribution of NFATc2 and NFATc1 to TNF-{alpha} Gene Expression in T Cells. J. Immunol. 180: 319-326 [Abstract] [Full Text]  
  • Klein, M., Klein-Hessling, S., Palmetshofer, A., Serfling, E., Tertilt, C., Bopp, T., Heib, V., Becker, M., Taube, C., Schild, H., Schmitt, E., Stassen, M. (2006). Specific and Redundant Roles for NFAT Transcription Factors in the Expression of Mast Cell-Derived Cytokines. J. Immunol. 177: 6667-6674 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»