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Targeting TNF and Its Family Members in Autoimmune/Inflammatory Disease

Call for Papers

Tumor necrosis factor (TNF), a pleiotropic cytokine mainly produced by activated macrophages, modulates a wide range of biological functions involving multiple organs. Besides its effects on tumor cell death, TNF is a key mediator of both acute and chronic inflammation. Since the description of TNF in 1970's and by consideration of structural homologies, more than 15 TNF-related cytokines have now been regrouped in a large family called TNF ligand superfamily (TNFSF), which interact with TNF receptor superfamily (TNFRSF) members. More than 150,000 scientific publications concerning TNF and its family members are available, demonstrating the strong interest of the scientific community in this molecule. In the last decade, TNF blocking agents have been developed for treatment of human disease and have been very successful in ameliorating disease signs and symptoms especially in patients suffering from autoimmune and chronic inflammatory disease like rheumatoid arthritis and Crohn's disease. Nonetheless, several aspects of these modulator effects remain enigmatic while appreciation of the role of other TNF family members in physiopathology of human autoimmune/inflammatory disease is increasing. Several important questions still remain: Why is a particular TNF blocker more successful than another? How to predict if the patient will benefit from TNF blocking therapy? Should biological monitoring of TNF inhibitor therapy be proposed in clinical practice to better control side-effects and/or cost of such therapies? Would it be of interest to target other TNF family members in inadequate responders to TNF blocking agents or in other indications where TNF inhibitors are not approved and perhaps contraindicated? What are the specific biological roles of other TNF superfamily members in comparison with TNF? Potential topics include, but are not limited to:

  • Analogies and differences between TNF blocking agents
  • Baseline predictors of response to TNF inhibitor therapy
  • Biological monitoring of TNF inhibitor therapy
  • Economic implications of TNF inhibitor therapy
  • Data supporting targeting of other TNF/TNFR superfamily members in human disease

Before submission authors should carefully read over the journal's Author Guidelines, which are located at http://www.hindawi.com/journals/mi/guidelines/. Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.hindawi.com/submit/journals/mi/tnf/ according to the following timetable:

Manuscript DueFriday, 31 May 2013
First Round of ReviewsFriday, 23 August 2013
Publication DateFriday, 18 October 2013

Lead Guest Editor

  • Sophie Desplat-Jégo, Autoimmune and Chronic Inflammatory Disease Exploration Group, Laboratory of Immunology, Hôpital de la Conception, University Hospital of Marseille, Aix Marseille University, France

Guest Editors

  • Linda Burkly, Biogen Idec, Inc., 12 Cambridge Center, Cambridge, MA 02142, USA
  • Chaim Putterman, Division of Rheumatology, Albert Einstein College of Medicine and Montefiore Medical Center, Bronx, NY10461, USA