Antibody-mediated inhibition of TNFR1 attenuates disease in a mouse model of multiple sclerosis
Tumour necrosis factor (TNF) is a proinflammatory cytokine that is known to regulate inflammation in a number of autoimmune diseases, including multiple sclerosis (MS). Although targeting of TNF in models of MS has been successful, the pathological role of TNF in MS remains unclear due to clinical t...
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| Veröffentlicht in: | PloS one 2014-02, Vol.9 (2), p.e90117-e90117 |
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| creator | Williams, Sarah K Maier, Olaf Fischer, Roman Fairless, Richard Hochmeister, Sonja Stojic, Aleksandar Pick, Lara Haar, Doreen Musiol, Sylvia Storch, Maria K Pfizenmaier, Klaus Diem, Ricarda |
| description | Tumour necrosis factor (TNF) is a proinflammatory cytokine that is known to regulate inflammation in a number of autoimmune diseases, including multiple sclerosis (MS). Although targeting of TNF in models of MS has been successful, the pathological role of TNF in MS remains unclear due to clinical trials where the non-selective inhibition of TNF resulted in exacerbated disease. Subsequent experiments have indicated that this may have resulted from the divergent effects of the two TNF receptors, TNFR1 and TNFR2. Here we show that the selective targeting of TNFR1 with an antagonistic antibody ameliorates symptoms of the most common animal model of MS, experimental autoimmune encephalomyelitis (EAE), when given following both a prophylactic and therapeutic treatment regime. Our results demonstrate that antagonistic TNFR1-specific antibodies may represent a therapeutic approach for the treatment of MS in the future. |
| doi_str_mv | 10.1371/journal.pone.0090117 |
| format | Article |
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Although targeting of TNF in models of MS has been successful, the pathological role of TNF in MS remains unclear due to clinical trials where the non-selective inhibition of TNF resulted in exacerbated disease. Subsequent experiments have indicated that this may have resulted from the divergent effects of the two TNF receptors, TNFR1 and TNFR2. Here we show that the selective targeting of TNFR1 with an antagonistic antibody ameliorates symptoms of the most common animal model of MS, experimental autoimmune encephalomyelitis (EAE), when given following both a prophylactic and therapeutic treatment regime. Our results demonstrate that antagonistic TNFR1-specific antibodies may represent a therapeutic approach for the treatment of MS in the future.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0090117</identifier><identifier>PMID: 24587232</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Analysis ; Animal models ; Animals ; Antibodies ; Antibodies - pharmacology ; Autoimmune diseases ; Biology ; Clinical trials ; Cytokines ; Disease ; Disease Models, Animal ; Encephalomyelitis, Autoimmune, Experimental - genetics ; Encephalomyelitis, Autoimmune, Experimental - immunology ; Encephalomyelitis, Autoimmune, Experimental - pathology ; Encephalomyelitis, Autoimmune, Experimental - therapy ; Experimental allergic encephalomyelitis ; Female ; Gene Expression ; Immunology ; Immunotherapy ; Inflammation ; Inhibition ; Medical research ; Medicine ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Molecular Targeted Therapy ; Multiple sclerosis ; Multiple Sclerosis - genetics ; Multiple Sclerosis - immunology ; Multiple Sclerosis - pathology ; Multiple Sclerosis - therapy ; Nervous system ; Neurodegeneration ; Neurology ; Oncology ; Paralysis ; Pathology ; Receptors ; Receptors, Tumor Necrosis Factor, Type I - antagonists & inhibitors ; Receptors, Tumor Necrosis Factor, Type I - deficiency ; Receptors, Tumor Necrosis Factor, Type I - genetics ; Receptors, Tumor Necrosis Factor, Type II - antagonists & inhibitors ; Receptors, Tumor Necrosis Factor, Type II - deficiency ; Receptors, Tumor Necrosis Factor, Type II - genetics ; Rheumatoid arthritis ; Rodents ; Spinal cord ; TNF inhibitors ; Tumor necrosis factor ; Tumor necrosis factor receptors ; Tumor necrosis factor-TNF ; Tumors</subject><ispartof>PloS one, 2014-02, Vol.9 (2), p.e90117-e90117</ispartof><rights>COPYRIGHT 2014 Public Library of Science</rights><rights>2014 Williams et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. 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Our results demonstrate that antagonistic TNFR1-specific antibodies may represent a therapeutic approach for the treatment of MS in the future.</description><subject>Analysis</subject><subject>Animal models</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Antibodies - pharmacology</subject><subject>Autoimmune diseases</subject><subject>Biology</subject><subject>Clinical trials</subject><subject>Cytokines</subject><subject>Disease</subject><subject>Disease Models, Animal</subject><subject>Encephalomyelitis, Autoimmune, Experimental - genetics</subject><subject>Encephalomyelitis, Autoimmune, Experimental - immunology</subject><subject>Encephalomyelitis, Autoimmune, Experimental - pathology</subject><subject>Encephalomyelitis, Autoimmune, Experimental - therapy</subject><subject>Experimental allergic encephalomyelitis</subject><subject>Female</subject><subject>Gene 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One</addtitle><date>2014-02-28</date><risdate>2014</risdate><volume>9</volume><issue>2</issue><spage>e90117</spage><epage>e90117</epage><pages>e90117-e90117</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Tumour necrosis factor (TNF) is a proinflammatory cytokine that is known to regulate inflammation in a number of autoimmune diseases, including multiple sclerosis (MS). Although targeting of TNF in models of MS has been successful, the pathological role of TNF in MS remains unclear due to clinical trials where the non-selective inhibition of TNF resulted in exacerbated disease. Subsequent experiments have indicated that this may have resulted from the divergent effects of the two TNF receptors, TNFR1 and TNFR2. Here we show that the selective targeting of TNFR1 with an antagonistic antibody ameliorates symptoms of the most common animal model of MS, experimental autoimmune encephalomyelitis (EAE), when given following both a prophylactic and therapeutic treatment regime. Our results demonstrate that antagonistic TNFR1-specific antibodies may represent a therapeutic approach for the treatment of MS in the future.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24587232</pmid><doi>10.1371/journal.pone.0090117</doi><tpages>e90117</tpages><oa>free_for_read</oa></addata></record> |
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| issn | 1932-6203 1932-6203 |
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| source | PLoS; MEDLINE; Full-Text Journals in Chemistry (Open access); DOAJ Directory of Open Access Journals; PubMed Central; EZB Electronic Journals Library |
| subjects | Analysis Animal models Animals Antibodies Antibodies - pharmacology Autoimmune diseases Biology Clinical trials Cytokines Disease Disease Models, Animal Encephalomyelitis, Autoimmune, Experimental - genetics Encephalomyelitis, Autoimmune, Experimental - immunology Encephalomyelitis, Autoimmune, Experimental - pathology Encephalomyelitis, Autoimmune, Experimental - therapy Experimental allergic encephalomyelitis Female Gene Expression Immunology Immunotherapy Inflammation Inhibition Medical research Medicine Mice Mice, Inbred C57BL Mice, Knockout Molecular Targeted Therapy Multiple sclerosis Multiple Sclerosis - genetics Multiple Sclerosis - immunology Multiple Sclerosis - pathology Multiple Sclerosis - therapy Nervous system Neurodegeneration Neurology Oncology Paralysis Pathology Receptors Receptors, Tumor Necrosis Factor, Type I - antagonists & inhibitors Receptors, Tumor Necrosis Factor, Type I - deficiency Receptors, Tumor Necrosis Factor, Type I - genetics Receptors, Tumor Necrosis Factor, Type II - antagonists & inhibitors Receptors, Tumor Necrosis Factor, Type II - deficiency Receptors, Tumor Necrosis Factor, Type II - genetics Rheumatoid arthritis Rodents Spinal cord TNF inhibitors Tumor necrosis factor Tumor necrosis factor receptors Tumor necrosis factor-TNF Tumors |
| title | Antibody-mediated inhibition of TNFR1 attenuates disease in a mouse model of multiple sclerosis |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-07T18%3A26%3A45IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Antibody-mediated%20inhibition%20of%20TNFR1%20attenuates%20disease%20in%20a%20mouse%20model%20of%20multiple%20sclerosis&rft.jtitle=PloS%20one&rft.au=Williams,%20Sarah%20K&rft.date=2014-02-28&rft.volume=9&rft.issue=2&rft.spage=e90117&rft.epage=e90117&rft.pages=e90117-e90117&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0090117&rft_dat=%3Cgale_plos_%3EA478787959%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1503272017&rft_id=info:pmid/24587232&rft_galeid=A478787959&rft_doaj_id=oai_doaj_org_article_d22907a816ca48d2a37e88deabdc6de2&rfr_iscdi=true |