European Working Party on Systemic Lupus Erythematosus: A 15-year report

2006 ◽  
Vol 5 (8) ◽  
pp. 549-553 ◽  
Author(s):  
Ricard Cervera ◽  
Josep Font ◽  
Yehuda Shoenfeld
Lupus ◽  
2001 ◽  
Vol 10 (12) ◽  
pp. 892-894 ◽  
Author(s):  
R Cervera ◽  
M A Khamashta ◽  
J Font ◽  
G RV Hughes ◽  

Lupus ◽  
2009 ◽  
Vol 18 (10) ◽  
pp. 884-888 ◽  
Author(s):  
G Zandman-Goddard ◽  
M Blank ◽  
Y Shoenfeld

This article is an update on the clinical and research data available on systemic lupus erythematosus (SLE) and intravenous immunoglobulin (IVIg) therapy that includes some studies performed under the umbrella of the European Working Party on SLE. Various mechanisms of IVIg may play a role, some synergistically, in the modulation of SLE. Recently it has been suggested that IVIg also suppresses the expansion of autoreactive B lymphocytes through signalling of the FcgRIIB, idiotype-mediated inhibition of B cell receptors and neutralisation of cytokines such as the B cell survival factors (B cell activation factor (BAFF and APRIL). In case reports and in open trials, high-dose IVIg (2 g/kg over a 5-day period) has consistently been shown to be a beneficial and safe adjunct therapeutic agent for over 20 manifestations in patients with SLE. It can be given as a first choice of therapy in some cases, for example, in neurological involvement and in those patients who refuse certain immunosuppressive agents such as cyclophosphamide, or in patients who have concomitant infections. Furthermore, IVIg may have a steroid-sparing effect although this characteristic needs further investigation. Specific IVIg (an anti-idiotype to anti-DNA, phosphorylcholine and antiphospholipids) has been shown to be effective in experimental murine models. Hence, extractable IVIg that is directed to the specific pathogenic immunoglobulins will enable the more specific therapy for patients with lupus.


Lupus ◽  
2009 ◽  
Vol 18 (10) ◽  
pp. 878-883 ◽  
Author(s):  
GD Sebastiani ◽  
M Galeazzi

Understanding the pathogenesis of systemic lupus erythematosus (SLE) remains a considerable challenge. Multiple abnormalities of both the innate and adaptive immune system have been described and, furthermore, immunological dysfunction precedes clinical presentation by many years. There is a strong genetic basis to SLE, which means that genetic studies can play a key role in furthering our understanding of this disease. Because susceptibility variants are present from birth and are unaffected by the course of the disease, or by its treatment, genetic analysis is, perhaps uniquely, capable of identifying fundamental, causative, disease mechanisms. In this article, we review our SLE immunogenetic studies performed in collaboration with the European Working Party on Systemic Lupus Erythematosus. By considering the results of our research and the recent advances obtained by genome-wide associations’ studies, we can begin to understand how dysregulation at a number of key immunological steps may predispose to the development of SLE.


Lupus ◽  
2009 ◽  
Vol 18 (10) ◽  
pp. 930-932 ◽  
Author(s):  
C Vasconcelos ◽  
R Cervera

The studies developed by the European Working Party on Systemic Lupus Erythematosus and the European Forum on Antiphospholipid Antibodies stress the importance of the creation of international networks devoted to the study of autoimmune diseases and the need for centres of excellence in the management of these conditions. This article analyses the importance of such centres and networks in Europe.


2013 ◽  
Vol 72 (Suppl 3) ◽  
pp. A903.2-A903
Author(s):  
R. F. Van Vollenhoven ◽  
M. Mosca ◽  
G. Bertsias ◽  
A. Kuhn ◽  
K. Lerström ◽  
...  

Author(s):  
Francis R. Comerford ◽  
Alan S. Cohen

Mice of the inbred NZB strain develop a spontaneous disease characterized by autoimmune hemolytic anemia, positive lupus erythematosus cell tests and antinuclear antibodies and nephritis. This disease is analogous to human systemic lupus erythematosus. In ultrastructural studies of the glomerular lesion in NZB mice, intraglomerular dense deposits in mesangial, subepithelial and subendothelial locations were described. In common with the findings in many examples of human and experimental nephritis, including many cases of human lupus nephritis, these deposits were amorphous or slightly granular in appearance with no definable substructure.We have recently observed structured deposits in the glomeruli of NZB mice. They were uncommon and were found in older animals with severe glomerular lesions by morphologic criteria. They were seen most commonly as extracellular elements in subendothelial and mesangial regions. The deposits ranged up to 3 microns in greatest dimension and were often adjacent to deposits of lipid-like round particles of 30 to 250 millimicrons in diameter and with amorphous dense deposits.


2000 ◽  
Vol 6 (7) ◽  
pp. 821-825 ◽  
Author(s):  
ELIZABETH LERITZ ◽  
JASON BRANDT ◽  
MELISSA MINOR ◽  
FRANCES REIS-JENSEN ◽  
MICHELLE PETRI

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