Skip Navigation



Rheumatology Advance Access published online on August 10, 2004
Rheumatology, doi:10.1093/rheumatology/keh353
Rheumatology © British Society for Rheumatology 2004; all rights reserved
This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
43/11/1357    most recent
keh353v1
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 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 arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Schotte, H.
Right arrow Articles by Schlüter, B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Schotte, H.
Right arrow Articles by Schlüter, B.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Received May 5, 2004
Accepted July 6, 2004

Original Papers

Interleukin-10 promoter microsatellite polymorphisms in systemic lupus erythematosus: association with the anti-Sm immune response

H. Schotte 1*, M. Gaubitz 1, P. Willeke 1, N. Tidow 2, G. Assmann 2, W. Domschke 1, B. Schlüter 2

1 Medizinische Klinik und Poliklinik B, Universitätsklinikum Münster, Germany
2 Institut für Klinische Chemie und Laboratoriumsmedizin, Universitätsklinikum Münster, Germany

* To whom correspondence should be addressed. E-mail: h.schotte{at}uni-muenster.de.


  Abstract

Objectives. Overproduction of interleukin-10 (IL-10) is a pivotal feature in the pathophysiology of systemic lupus erythematosus (SLE). In vitro IL-10 secretion has previously been related to haplotypes of the IL-10 promoter microsatellite polymorphisms IL10.R and IL10.G. Published data concerning the association of IL10.G alleles with susceptibility to SLE are inconsistent in different ethnic populations. We analysed the association of IL-10 promoter microsatellite polymorphisms with disease susceptibility and manifestations in German Caucasian patients with SLE.

Methods. Two hundred and ten (210) SLE patients fulfilling the 1997 revised ACR criteria and 158 ethnically, age- and sex-matched healthy controls were genotyped for the IL-10 promoter microsatellite polymorphisms by fragment length analysis. Haplotypes were reconstructed using a Bayesian coalescent theory-based method with PHASE software. Allele and haplotype distributions were compared between patients and controls and between subgroups of patients with different clinical and immunopathological findings.

Results. In the study population no significant associations of individual IL10.R and G alleles or their haplotypes with susceptibility to SLE or major clinical manifestations were observed. By contrast, alleles G14 and G15 and haplotypes R2-G14 and R2-G15 were significantly over-represented in anti-Sm antibody-positive patients.

Conclusions. The IL-10 promoter microsatellite polymorphisms and their haplotypes do not constitute a major risk factor for SLE in German Caucasians. However, the identification of genetic markers such as the IL-10 high-response haplotype R2-G14 predisposing for the production of anti-Sm antibodies may help to elucidate the conditions that lead to the development of SLE.

Keywords: Systemic lupus erythematosus; Interleukin-10; Promoter microsatellite polymorphisms; Anti-Sm antibodies; German Caucasian patients.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




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.