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עמוד בית
Fri, 01.11.24

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October 2015
Lone Sølling Avnon MD, Alexander Smoliakov MD, Igor Sinelko MD and Mahmoud Abu-Shakra MD
June 2015
Sandy Mpho Mosenye MBChB, Josè Antonio Moulton Alvarez MD, Rafael Enrique Cruz Abascal MD, Matthew N. Tanko MBBS FMCPath (Nig), Francesca Cainelli MD and Sandro Vento MD
April 2015
Mathilde Versini MD, Giorgia Bizzaro BSc and Yehuda Shoenfeld MD FRCP MaACR
Lior Zeller MD, Leonid Barski MD, Elena Shleyfer MD, Uri Netz MD, Vered Stavi MD and Mahmoud Abu-Shakra MD
March 2015
Carlo Perricone MD, Monica Pendolino MD, Marta Olivieri MD, Fabrizio Conti MD PhD, Guido Valesini MD and Cristiano Alessandri MD

Abstract

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by multisystem involvement due to immune dysregulation. Neuropsychiatric systemic lupus erythematosus (NPSLE) includes neurological syndromes involving the central, peripheral and autonomic nervous system, as well as psychiatric syndromes observed in patients with SLE in which other causes have been excluded. The pathogenesis of NPSLE has been attributed to many different mechanisms. In particular, autoantibody-mediated vasculopathy seems to play a major role in the pathogenesis of the clinical features. Several autoantibody specificities have been reported in the serum and cerebrospinal fluid of NPSLE patients. Recently, we demonstrated an association between serum anti-endothelial antibodies (AECA) and psychosis or depression in SLE patients, strengthening the notion of a possible role of this class of autoantibodies in the pathogenesis of the disease. The study of these autoantibodies could be a useful diagnostic and prognostic tool in patients with NPSLE.

 

 

February 2015
Daphna Paran MD and Yaakov Naparstek MD
In the past decade we have witnessed a dramatic change in the management of autoimmune diseases, such as rheumatoid arthritis and spondyloarthropathies, due to the development of new biologic drugs designed to target key mediators in the autoimmune process. However, the development of similar target-specific drugs for the management of SLE has not been as successful. The B cell has long been considered central to the pathogenesis of SLE and has been regarded as an important target for biologic drugs. Several B cell-targeted drugs have been developed and although the mechanisms seem promising, most of the studies published to date have failed to achieve their primary endpoints, leading to an ongoing debate regarding the role of B cell therapy in SLE. The present report discusses the pros and cons of B cell-targeted therapy in SLE, reviews the clinical studies, and offers possible explanations for the discrepancies between randomized control studies and real-life experience. 

 
Siniša Roginic MD, Alan Jelic MD, Asja Stipic-Markovic MD PhD, Artukovic Marinko MD, Irena N. Artukovic MD and Martinovic-Kaliterna Dusanka MD PhD
October 2014
Carlo Perricone MD, Elias Toubi MD, Guido Valesini MD and Yehuda Shoenfeld MD FRCP (Hon.) MaACR
Orit Barrett MD, Ella Abramovich MD, Jacob Dreiher MD MPH, Victor Novack MD PhD and Mahmoud Abu-Shakra MD
Laura Andreoli MD, Rossella Reggia MD, Lara Pea MD, Micol Frassi MD, Alessandra Zanola PhD, Stefania Cartella MD, Franco Franceschini MD and Angela Tincani MD
August 2014
Daniel Elbirt MD*, Ilan Asher MD*, Keren Mahlab-Guri MD, Shira Bezalel-Rosenberg MD, Victor Edelstein MD and Zev Sthoeger MD

Background: Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by disturbance of the innate and adaptive immune systems with the production of autoantibodies by stimulated B lymphocytes. The BLyS protein (B lymphocyte stimulator) is secreted mainly by monocytes and activated T cells and is responsible for the proliferation, maturation and survival of B cells.

Objectivs: To study sera BLyS level and its clinical significance in Israeli lupus patients over time.

Methods: The study population included 41 lupus patients (8 males, 33 females; mean age 35.56 ± 15.35 years) and 50 healthy controls. The patients were followed for 5.02 ± 1.95 years. We tested 221 lupus sera (mean 5.4 samples/patient) and 50 normal sera for BLyS levels by a capture ELISA. Disease activity was determined by the SLEDAI score.

Results: Sera BLyS levels were significantly higher in SLE patients than in controls (3.37 ± 3.73 vs. 0.32 ± 0.96 ng/ml, P < 0.05). BLyS levels were high in at least one sera sample in 80.5% of the patients but were normal in all sera in the control group. There was no correlation between sera BLyS and anti-ds-DNA autoantibody levels. BLyS levels fluctuated over time in sera of lupus patients with no significant correlation to disease activity.

Conclusions: Most of our lupus patients had high sera BLyS levels, suggesting a role for BLyS in the pathogenesis and course of SLE. Our results support the current novel approach of targeting BLyS (neutralization by antibodies or soluble receptors) in the treatment of active lupus patients.

May 2014
April 2014
Shira Bezalel MD, Keren Mahlab Guri MD, Daniel Elbirt MD, Ilan Asher MD and Zev Moshe Sthoeger MD
 Type I interferons (IFN) are primarily regarded as an inhibitor of viral replication. However, type I IFN, mainly IFNα, has a major role in activation of both the innate and adaptive immune systems. Systemic lupus erythematosus (SLE) is a chronic, multi-systemic, inflammatory autoimmune disease with undefined etiology. SLE is characterized by dysregulation of both the innate and the adaptive immune systems. An increased expression of type I IFN-regulated genes, termed IFN signature, has been reported in patients with SLE. We review here the role of IFNα in the pathogenesis and course of SLE and the possible role of IFNα inhibition as a novel treatment for lupus patients.

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