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Rheumatology Advance Access originally published online on May 31, 2005
Rheumatology 2005 44(8):962-964; doi:10.1093/rheumatology/keh702
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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

Annus mirabilis—a guide to the 6th European Lupus Meeting, 3–5 March 2005

A. Rahman, S. J. Bowman1, I. P. Giles, Y. Ioannou and D. A. Isenberg

Centre for Rheumatology, Division of Medicine, University College London, London and 1 Department of Rheumatology, University Hospital, Birmingham, UK.

Correspondence to: A. Rahman, Centre for Rheumatology, Division of Medicine, University College London, Arthur Stanley House, 40–50 Tottenham Street, London W1T 4NJ, UK. E-mail: anisur.rahman@ucl.ac.uk

KEY WORDS: Systemic lupus erythematosus, Conference report

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

The year 2005 will be an annus mirabilis for systemic lupus erythematosus (SLE). Several major double-blind controlled trials involving hundreds of patients with lupus will be getting started. These trials include a comparison of mycophenolate and cyclophosphamide in lupus nephritis, the use of the humanized anti-CD20 monoclonal antibody, CTLA-4 Ig, anti-BLys and a DNA antibody-binding peptide. These potential therapeutic advances have been possible due to basic science research, which has illuminated many facets of the immunopathogenesis of SLE.

At the 6th European Lupus Meeting, held in London at the Royal College of Physicians on 3–5 March 2005, these clinical and basic science aspects of SLE were brought together with detailed reviews of the immunogenetics of lupus and the roles of complement, cytokines, B and T lymphocytes and antibodies in the pathogenesis of the disease, and detailed assessments of the optimal management of lupus in the kidney, brain, lungs, skin and . . . [Full Text of this Article]

Clinical aspects of lupus

Basic science and the pathogenesis of SLE

Conclusion


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