Skip Navigation


Human Molecular Genetics Advance Access originally published online on February 5, 2004
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
13/suppl_1/R143    most recent
ddh076v1
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
Google Scholar
Right arrow Articles by Prokunina, L.
Right arrow Articles by Alarcon-Riquelme, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Prokunina, L.
Right arrow Articles by Alarcon-Riquelme, M.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Human Molecular Genetics, 2004, Vol. 13, Review Issue 1 R143-R148
DOI: 10.1093/hmg/ddh076

The genetic basis of systemic lupus erythematosus—knowledge of today and thoughts for tomorrow

Ludmila Prokunina and Marta Alarcon-Riquelme*

Department of Genetics and Pathology, Section for Medical Genetics, Rudbeck Laboratory, Uppsala University, Dag Hammarskjölds väg 20, 751 85, Uppsala, Sweden

Systemic lupus erythematosus (SLE) is a chronic rheumatic disease with an autoimmune etiology. Nuclear components of the cells are the main targets of the autoimmune reaction, affecting virtually any organ in the body. SLE is also called a prototype disease due to a substantial overlap in its clinical symptoms with other autoimmune diseases. Therefore the understanding of the mechanisms underlying SLE may contribute to advances in studies and development of new treatments for several autoimmune diseases. SLE is a complex disease with both genetic factors (mutations or susceptibility alleles) and environmental factors (infections, drugs, stress, exposures, etc.) contributing to its development. In this article we will give an overview of the latest findings in genetics of SLE, concentrating on the two most interesting and promising pathways: the PD-1 and the interferon pathways.

* To whom correspondence should be addressed. Tel: +46 184714805; Fax: +46 184714808; Email: marta.alarcon{at}genpat.uu.se


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
J. Mol. Diagn.Home page
S. C. Fossey, C. L. Vnencak-Jones, N. J. Olsen, S. Sriram, G. Garrison, X. Deng, P. S. Crooke III, and T. M. Aune
Identification of Molecular Biomarkers for Multiple Sclerosis
J. Mol. Diagn., April 1, 2007; 9(2): 197 - 204.
[Abstract] [Full Text] [PDF]


Home page
Hum Mol GenetHome page
Y. Hitomi, N. Tsuchiya, A. Kawasaki, J. Ohashi, T. Suzuki, C. Kyogoku, T. Fukazawa, S. Bejrachandra, U. Siriboonrit, D. Chandanayingyong, et al.
CD72 polymorphisms associated with alternative splicing modify susceptibility to human systemic lupus erythematosus through epistatic interaction with FCGR2B
Hum. Mol. Genet., December 1, 2004; 13(23): 2907 - 2917.
[Abstract] [Full Text] [PDF]


Home page
Rheumatology (Oxford)Home page
H. Schotte, M. Gaubitz, P. Willeke, N. Tidow, G. Assmann, W. Domschke, and B. Schluter
Interleukin-10 promoter microsatellite polymorphisms in systemic lupus erythematosus: association with the anti-Sm immune response
Rheumatology, November 1, 2004; 43(11): 1357 - 1363.
[Abstract] [Full Text] [PDF]


Home page
Hum Mol GenetHome page
M. Farrall
Quantitative genetic variation: a post-modern view
Hum. Mol. Genet., April 1, 2004; 13(90001): R1 - 7.
[Abstract] [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.