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 Google Scholar
Google Scholar
Right arrow Articles by Rödel, J.
Right arrow Articles by Straube, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Rödel, J.
Right arrow Articles by Straube, E.

 Previous Article  |  Next Article 

Infection and Immunity, November 2002, p. 6140-6146, Vol. 70, No. 11
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.11.6140-6146.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Role of Interferon-Stimulated Gene Factor 3{gamma} and Beta Interferon in HLA Class I Enhancement in Synovial Fibroblasts upon Infection with Chlamydia trachomatis

Jürgen Rödel,1* Heinz Vogelsang,2 Katrin Prager,1 Matthias Hartmann,1 Karl-Hermann Schmidt,1 and Eberhard Straube1

Institute of Medical Microbiology,1 Institute of Clinical Chemistry, Friedrich Schiller University of Jena, D-07740 Jena, Germany2

Received 24 April 2002/ Returned for modification 11 June 2002/ Accepted 5 August 2002

Chlamydia trachomatis infection can cause reactive arthritis that is associated with the persistence of chlamydial organisms in the joint. Fibroblasts of the synovial membrane represent host cells for Chlamydia during articular infection. In this study we investigated the expression of HLA class I molecules in synovial fibroblasts following infection with C. trachomatis D. The expression of HLA class I heavy chain (HLA-I) was up-regulated in infected cultures as shown by reverse transcription-PCR and immunoblotting. The increase in cell surface expression of HLA-I and ß2 microglobulin on infected fibroblasts was demonstrated by flow cytometric analysis. Suppression of enhanced production of interferon-stimulated gene factor 3{gamma} (ISGF3{gamma}) in infected cell cultures by antisense oligonucleotide treatment reduced the level of HLA-I. Blocking antibodies to beta interferon (IFN-ß) inhibited the Chlamydia-induced enhancement of both ISGF3{gamma} and HLA-I. These findings show that the up-regulation of HLA-I in synovial fibroblasts infected with C. trachomatis is caused by the induction of IFN-ß, which in turn stimulates the synthesis of ISGF3{gamma}, a transcription factor participating in the regulation of the HLA-I gene. The IFN-ß-mediated expression of HLA-I on Chlamydia-infected cells may be a regulatory factor in the immune response in chlamydial infections.

* Corresponding author. Mailing address: Institute of Medical Microbiology, Friedrich Schiller University of Jena, Semmelweisstr. 4, D-07740 Jena, Germany. Phone: 49-3641-933105. Fax: 49-3641-933474. E-mail: juergen.roedel{at}med.uni-jena.de.

Editor: J. D. Clements

Infection and Immunity, November 2002, p. 6140-6146, Vol. 70, No. 11
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.11.6140-6146.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.





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