Reverse Signaling Contributes to Control of Chronic Inflammation by Anti-TNF Therapeutics
العنوان: | Reverse Signaling Contributes to Control of Chronic Inflammation by Anti-TNF Therapeutics |
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المؤلفون: | Ernő Duda, Orsolya Sipos, Kata Filkor, Tanja Kalic, Annamária Török |
المصدر: | Antibodies, Vol 4, Iss 2, Pp 123-140 (2015) Antibodies Volume 4 Issue 2 Pages 123-140 |
بيانات النشر: | MDPI AG, 2015. |
سنة النشر: | 2015 |
مصطلحات موضوعية: | lcsh:Immunologic diseases. Allergy, Agonist, Cell signaling, medicine.drug_class, reverse signal, Immunology, tumor necrosis factor (TNF), Inflammation, macrophage, Biology, Monoclonal antibody, Drug Discovery, medicine, Immunology and Allergy, Macrophage, TNF receptor, autoimmune, Fusion protein, Ectodomain, inflammation, Cancer research, Tumor necrosis factor alpha, monoclonal antibodies, medicine.symptom, lcsh:RC581-607 |
الوصف: | Anti-tumor necrosis factor (TNF) monoclonal antibodies and TNF receptor ectodomain fusion protein are in clinical use to neutralize circulating TNF and ameliorate symptoms of many autoimmune diseases and pathological conditions with chronic inflammation. In this paper we present data to prove that reverse signaling, elicited by agonist molecules interacting with the membrane-bound TNF of myeloid cells, significantly contributes to the therapeutic effect of these anti-TNF medicines. Interaction of agonist monoclonals with cell surface TNF significantly attenuates the expression of pro-inflammatory cytokines and induces changes in the production of extracellular and intracellular signaling molecules. This phenomenon is not dependent on the Fc portion of antibodies as Fab constructs are as efficient as full antibody molecules. |
وصف الملف: | application/pdf |
تدمد: | 2073-4468 |
URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::7b44d8a5622e9d7a2b71917a3c42f2ab https://doi.org/10.3390/antib4020123 |
حقوق: | OPEN |
رقم الأكسشن: | edsair.doi.dedup.....7b44d8a5622e9d7a2b71917a3c42f2ab |
قاعدة البيانات: | OpenAIRE |
تدمد: | 20734468 |
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