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עמוד בית
Fri, 05.12.25

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January 2008
E. Toubi


Among the several mechanisms that play a role in maintaining peripheral self-tolerance is the existence of a unique CD4+CD25+ population of naturally occurring regulatory T cells, which actively prevent both the activation and the effector function of autoreactive T cells that have escaped different mechanisms of tolerance. Many studies have shown the benefit of targeting this cell population by restoring self-tolerance. Therapies that could possibly increase the suppressive ability of T regulatory cells were proven to improve the course of autoimmune diseases.

G. Zandman-Goddard and Y. Shoenfeld
 

Controlling iron/oxygen chemistry in biology depends on multiple genes, regulatory messenger RNA structures, signaling pathways and protein catalysts. Ferritin synthesis is regulated by cytokines (tumor necrosis factor-alpha and interleukin-1α) at various levels (transcriptional, post-transcriptional, translational) during development, cellular differentiation, proliferation and inflammation. The cellular response by cytokines to infection stimulates the expression of ferritin genes. The immunological actions of ferritin include binding to T lymphocytes, suppression of the delayed-type hypersensitivity, suppression of antibody production by B lymphocytes, and decreased phagocytosis of granulocytes. Thyroid hormone, insulin and insulin growth factor-1 are involved in the regulation of ferritin at the mRNA level. Ferritin and iron homeostasis are implicated in the pathogenesis of many disorders, including diseases involved in iron acquisition, transport and storage (primary hemochromatosis) as well as in atherosclerosis, Parkinson's disease, Alzheimer disease, and restless leg syndrome. Mutations in the ferritin gene cause the hereditary hyperferritinemia-cataract syndrome and neuroferritinopathy. Hyperferritinemia is associated with inflammation, infections and malignancies, and in systemic lupus erythematosus correlates with disease activity. Some evidence points to the importance of hyperferritinemia in dermatomyositis and multiple sclerosis, but further mechanistic investigations are warranted.

January 2007
avital avriel, daniel flusser, mahmoud abu shakra, sima halevi, shaul sukenik, avriel, flusser, abu shakra, halevi, sukenik, psoriasis, psoriatic arthritis, systemic lupus eythematosus
February 2006
J. Rovensky

Klinefelter's syndrome, which occurs in males, is not a rare gonosomal aberration. The disorder is characterized by micro-orchidism.

October 2005
X. Giakoumi, M. Tsironi, C. Floudas, E. Polymeropoylos, E. Papalambros and A. Aessopos
December 2004
E. Zebeede, U. Levinger and A. Weinberger
May 2002
Ori Efrati, MD, Asher Barak, MD, Jacob Yahav, MD, Lea Leibowitz, MD, Nathan Keller, MD and Yoram Bujanover, MD
April 2002
Rosalia Smolyakov, MD, Klaris Riesenberg, MD, Francisc Schlaeffer, MD, Abraham Borer, MD, Jacob Gilad, MD, Nechama Peled, MSc and Michael Alkan, MD
January 2002
Philip J. Hashkes, MD, MSc, Orit Friedland, MD and Yosef Uziel, MD, MSc
September 2001
Auli Toivanen, MD and Paavo Toivanen, MD

Reactive arthritis is a disease affecting mostly young adults. Owing to a greater general awareness the diagnosis has become more common during recent years. It is well established that ReA is caused by an infection, mostly in genetically susceptible individuals. The pathogenetic mechan­isms are still poorly understood, and the treatment rests mainly on anti-inflammatory drugs or steroids. Vigorous and early treatment of the triggering infection may prevent the develop­ment of ReA but this is rarely possible in everyday clinical practice. Despite its name, the disease should be considered as a general disorder that affects not only the joints. The prognosis is not as good as earlier believed, and relapses or chronic development are not unusual.

Larry W. Moreland, MD

There is accumulating evidence that tumor necrosis factor plays a major role in the pathogenesis of rheumatoid arthritis. Recent biotechnological advances have allowed for the development of agents that directly target TNF, a pro-inflammatory cytokine. In the last 2 years, the U.S. Food and Drug Administration and the European Union’s Commission of the European Communities have approved two biological agents for the treatment of refractory RA, etanercept and infliximab. Etanercept is a fusion protein, composed of the Fc portion of immunoglobulin G1 and the extracellular domain of a TNF receptor (p75). Infliximab is a chimeric monoclonal antibody composed of murine variable and human constant regions. In placebo-controlled trials, both agents have proven to be effective and well tolerated in PA patients.

Daniel Schapira, MD, DSc, Alexandra Balbir-Gurman, MD, Alicia Nachtigal, MD and Abraham Menachem Nahir, MD, PhD
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