• IMA sites
  • IMAJ services
  • IMA journals
  • Doctors card
  • Follow us
עמוד בית Fri, 23.08.19

October 2014


Editorial
Carlo Perricone MD, Elias Toubi MD, Guido Valesini MD and Yehuda Shoenfeld MD FRCP (Hon.) MaACR
Articles
Marcella Di Gangi MD, Giorgio Amato MD, Giovanni Converso MD, Alessia Benenati MD, Concetta Leonetti MD, Elisabetta Borella MD, Andrea Doria MD and Rosario Foti MD
Elisabetta Borella MD, Lavinia Palma MD, Margherita Zen MD, Silvano Bettio MD, Linda Nalotto MD, Mariele Gatto MD, Marta Domeneghetti MD, Luca Iaccarino MD, Leonardo Punzi and Andrea Doria MD
Autoinflammatory (AIF) and autoimmune (AIM) diseases are chronic immune disorders characterized by dysregulation of the immune system. Most AIF diseases are monogenic diseases which lead to hyperactivation of the inflammasome and release of pro-inflammatory cytokines, such as interleukin-1 (IL-1) and IL-18, resulting in tissue inflammation. Besides, the main feature of autoimmune diseases is the loss of tolerance of the adaptive immune cells against self antigens. Most AIF diseases are polygenic and numerous immune pathogens are involved in organ damage. The involvement of some AIF-associated mechanisms in AIM diseases, i.e., the activation of the inflammasome and the role of IL-1, was recently recognized. Moreover, some single nucleotide polymorphisms of the inflammasome genes have been proven to be involved in the development of AIF-related inflammatory features in autoimmune patients. These observations raise the possibility of using some anti-inflammatory drugs, like IL-1 antagonists, in autoimmune diseases with autoinflammatory features. 
Rina Aharoni PhD and Ruth Arnon PhD

A fundamental challenge for multiple sclerosis (MS) therapy is to promote repair and remyelination beyond their limited spontaneous extent. Glatiramer acetate (GA, Copaxone®), an approved treatment for MS, has been shown to induce immunomodulation as well as neuroprotection in the inflamed central nervous system (CNS) in MS and in its model, experimental autoimmune encephalomyelitis (EAE). Using electron microscopy, immunohistochemistry, and advanced magnetic resonance imaging, we have demonstrated diminished myelin damage in GA-treated mice, in both relapsing-remitting and chronic EAE, even when treatment was applied late after the disease exacerbation, suggesting repair. Furthermore, quantitative analysis indicated significant elevation in remyelinated axons in GA-treated compared to untreated EAE mice. To further prove that GA can promote myelination, we studied its effect in the developing naïve CNS, when injected postnatally. Immunohistochemical and ultrastructural analyses revealed significant increase in the number of myelinated axons, the thickness of the myelin encircling them, and the resulting g-ratios in the spinal cords of GA-injected mice compared to their phosphate-buffered saline-injected littermates. A prominent elevation in the amount of progenitor oligodendrocytes and their proliferation, as well as in mature oligodendrocytes, implied that the effect of GA is linked to the differentiation along the oligodendroglial cascade. Furthermore, a functional advantage in rotating rod test was exhibited by GA-injected mice over their littermates. These cumulative findings indicate that GA treatment affects myelination under inflammatory as well as non-inflammatory conditions, supporting the notion that the repair process in the CNS can be up-regulated by therapy.

Mathilde Versini MD, Gali Aljadeff BSc, Pierre-Yves Jeandel MD PhD and Yehuda Shoenfeld MD
Paola Triggianese MD, Maria D. Guarino MD, Eleonora Ballanti MD, Maria S. Chimenti MD PhD and Roberto Perricone MD
Yael Bar-On MD, Varda Shalev MD, Dahlia Weitzman PhD, Gabriel Chodick PhD and Howard Amital MD MHA
Tomer Bashi MD, Miri Blank PhD and Yehuda Shoenfeld MD FRCP
Orit Barrett MD, Ella Abramovich MD, Jacob Dreiher MD MPH, Victor Novack MD PhD and Mahmoud Abu-Shakra MD
María-Teresa Arango MSc, Shaye Kivity MD, Joab Chapman MD PhD and Yehuda Shoenfeld MD FRCP
Piercarlo Sarzi-Puttini MD and Fabiola Atzeni MD PhD
Marzia Dolcino PhD, Antonio Puccetti MD PhD, Andrea Ottria MD, Alessandro Barbieri PhD, Giuseppe Patuzzo MD PhD and Claudio Lunardi 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
Carlo Perricone MD, Shunit Rinkevich-Shop PhD, Miri Blank PhD, Natalie Landa-Rouben PhD, Cristiano Alessandri MD, Fabrizio Conti MD, PhD, Jonathan Leor MD, Yehuda Shoenfeld MD FRCP and Guido Valesini MD
Lucija Tomljenovic PhD, Maria-Teresa Arango MSc and Nancy Agmon-Levin MD
Serena Colafrancesco MD, Roberta Priori MD PhD, Cristiano Alessandri MD, Elisa Astorri MD PhD, Carlo Perricone MD, Miri Blank PhD, Nancy Agmon-Levin MD, Yehuda Shoenfeld MD FRCP MaACR and Guido Valesini MD
Cristina Rosário MD and Yehuda Shoenfeld, MD FRCP MaACR
M. Galeazzi, L. Bazzichi, G.D. Sebastiani, D. Neri, E. Garcia Gonzalez, N. Ravenni, L. Giovannoni, J. Wilton, M. Bardelli, C. Baldi, E. Selvi, A. Iuliano, G. Minisola, R. Caporali, E. Prisco and S. Bombardieri
Caterina De Carolis MD, Carlo Perricone MD and Roberto Perricone MD
הבהרה משפטית: כל נושא המופיע באתר זה נועד להשכלה בלבד ואין לראות בו ייעוץ רפואי או משפטי. אין הר"י אחראית לתוכן המתפרסם באתר זה ולכל נזק שעלול להיגרם. כל הזכויות על המידע באתר שייכות להסתדרות הרפואית בישראל. מדיניות פרטיות
ז'בוטינסקי 35 רמת גן, בניין התאומים 2 קומות 10-11, ת.ד. 3566, מיקוד 5213604. טלפון: 03-6100444, פקס: 03-5753303