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Rheumatology Advance Access originally published online on May 24, 2005
Rheumatology 2005 44(9):1086-1089; doi:10.1093/rheumatology/keh695
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© The Author 2005. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org

EDITORIAL

Experimental models of systemic lupus erythematosus: anti-dsDNA in murine lupus

M. Blank1 and Y. Shoenfeld1,2

1 Department of Medicine B and The Center for Autoimmune Diseases, Sheba Medical Center, Tel Hashomer, Sackler Faculty of Medicine and 2 Incumbent of the Laura Schwartz–Kipp chair for Autoimmunity, Tel Aviv University, Israel.

Correspondence to: Y. Shoenfeld, Department of Medicine B and Center for Autoimmune Diseases, Sheba Medical Center, Tel Hashomer, Israel 52621. E-mail: shoenfel@post.tau.ac.il

The first 150 words of the full text of this article appear below.

The aim of this editorial is to highlight the need for further insight into the network cascade leading to diverse serological, clinical and inflammatory manifestations and multiple organ damage in lupus, associated with anti-double-stranded DNA (anti-dsDNA) antibodies. Better understanding of the lupus network may serve as a basis to develop specific targeted therapy based on lessons from experimental lupus models.

Systemic lupus erythematosus (SLE) is an autoimmune disease of multifactorial etiology and diverse mechanisms. Although the disease is T-cell-dependent and antigen-driven, more than 100 autoantibodies were detected in the sera of lupus patients with differential correlation to disease activity [1, 2].

Many of the current autoantigen targets are derived from macromolecular structures such as chromatin (nucleosomes composed of dsDNA and histones), and small nuclear ribonucleoproteins (snRNPs) [3]. Using lupus-prone mice [(NZBxNZW)F1(BWF1) or (SWRxNZB)F1(SNF1)], Mohan et al. showed that the nucleosome . . . [Full Text of this Article]


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