Skip Navigation


Rheumatology Advance Access originally published online on June 22, 2004
Rheumatology 2004 43(9):1109-1115; doi:10.1093/rheumatology/keh267
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
43/9/1109    most recent
keh267v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (4)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Henriksson, G.
Right arrow Articles by Bredberg, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Henriksson, G.
Right arrow Articles by Bredberg, A.
Related Collections
Right arrow Sjogren's Syndrome
Right arrow Immunogenetics
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Rheumatology Vol. 43 No. 9 © British Society for Rheumatology 2004; all rights reserved

Paper

Enhanced DNA-dependent protein kinase activity in Sjögren's syndrome B cells

G. Henriksson, A. Sallmyr, L. Du, Å. Larsson1, R. Manthorpe2 and A. Bredberg

Department of Medical Microbiology, Lund University, Malmö University Hospital, 1 Department of Oral Pathology, Centre for Oral Health Sciences and 2 Department of Rheumatology, Sjögren's Syndrome Research Centre, Lund University, Malmö University Hospital, Malmö, Sweden.

Correspondence to: G. Henriksson, Department of Medical Microbiology, Malmö University Hospital, S-205 02 Malmö, Sweden. E-mail: gunnel.henriksson{at}mikrobiol.mas.lu.se

Objective. To examine the stress response, including the role of DNA-dependent protein kinase (DNA-PK), in B cells from Sjögren's syndrome (SS) patients.

Methods. B-cell lines were exposed to gamma radiation and then postincubated to allow inducible stress functions to develop. The magnitude of the DNA damage response was monitored with respect to DNA-PK phosphorylation of a p53 peptide, defence protein levels (Ku, DNA-PK catalytic subunit, ATM, p21 and p53) and flow cytometric determination of cell cycle phases and apoptosis.

Results. B cells from SS patients, compared with healthy controls, displayed enhancement of two stress functions in undamaged cells: DNA-PK kinase activity and apoptosis. In addition, SS showed enhanced cell cycle arrest in gamma-irradiated cells.

Conclusions. Strong kinase activity of DNA-PK, functioning not only in a DNA damage response but also in immunoglobulin gene rearrangement, may be an important component of the heightened stress response displayed by SS cells. In combination with recent reports, our data indicate that constitutional hyper-reactivity to danger signals is a basic pathogenetic factor in SS.

KEY WORDS: Sjögren's syndrome, DNA-dependent protein kinase, Ku protein, Stress response, Cell cycle arrest


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Rheumatology (Oxford)Home page
A. Bredberg, G. Henriksson, A. Larsson, R. Manthorpe, and A. Sallmyr
Sjogren's syndrome and the danger model
Rheumatology, August 1, 2005; 44(8): 965 - 970.
[Full Text] [PDF]


Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.