Anti-TNF-α Antibodies Suppress the Development of Experimental Autoimmune Myasthenia Gravis
To understand the role of TNF-α in the induction of experimental autoimmune myasthenia gravis (EAMG) and detect a possible effect of anti-TNF-α antibodies in the treatment of EAMG, anti-TNF-α antibodies were administrated intraperitoneally to Lewis rats twice per week for 5 weeks from the day of imm...
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| Veröffentlicht in: | Journal of autoimmunity 2002-12, Vol.19 (4), p.169-174 |
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| container_title | Journal of autoimmunity |
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| creator | Duan, Rui-Sheng Wang, Hua-Bing Yang, Jian-She Scallon, Bernie Link, Hans Xiao, Bao-Guo |
| description | To understand the role of TNF-α in the induction of experimental autoimmune myasthenia gravis (EAMG) and detect a possible effect of anti-TNF-α antibodies in the treatment of EAMG, anti-TNF-α antibodies were administrated intraperitoneally to Lewis rats twice per week for 5 weeks from the day of immunization with Torpedo AChR and complete Freund's adjuvant (CFA). Administration of anti-TNF-α antibodies resulted in lower incidence of EAMG, and in delayed onset and only mild muscle weakness compared with control EAMG rats. These mild clinical signs were accompanied by lower AChR-specific lymphocyte proliferation, down-regulated IFN-γ and IL-10, and up-regulated TGF-β. The lower levels of anti-AChR IgG, Ig2a and IgG2b and decreased anti-AChR IgG affinity were found in rats treated with anti-TNF-α antibodies. These results demonstrate that anti-TNF-α antibodies can suppress the induction and development of EAMG. |
| doi_str_mv | 10.1006/jaut.2002.0618 |
| format | Article |
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Administration of anti-TNF-α antibodies resulted in lower incidence of EAMG, and in delayed onset and only mild muscle weakness compared with control EAMG rats. These mild clinical signs were accompanied by lower AChR-specific lymphocyte proliferation, down-regulated IFN-γ and IL-10, and up-regulated TGF-β. The lower levels of anti-AChR IgG, Ig2a and IgG2b and decreased anti-AChR IgG affinity were found in rats treated with anti-TNF-α antibodies. These results demonstrate that anti-TNF-α antibodies can suppress the induction and development of EAMG.</description><identifier>ISSN: 0896-8411</identifier><identifier>EISSN: 1095-9157</identifier><identifier>DOI: 10.1006/jaut.2002.0618</identifier><identifier>PMID: 12473237</identifier><language>eng</language><publisher>London: Elsevier Ltd</publisher><subject>Animals ; Antibodies - immunology ; Biological and medical sciences ; Disease Models, Animal ; Diseases of striated muscles. Neuromuscular diseases ; Down-Regulation ; experimental autoimmune myasthenia gravis, anti-TNF-α antibodies, cytokine, anti-AChR antibodies ; Female ; General aspects ; Immunopathology ; Interferon-gamma - immunology ; Interleukin-10 - immunology ; Medical sciences ; Myasthenia Gravis, Autoimmune, Experimental - immunology ; Myasthenia Gravis, Autoimmune, Experimental - prevention & control ; Neurology ; Rats ; Rats, Inbred Lew ; Receptors, Nicotinic - metabolism ; T-Lymphocytes - immunology ; Torpedo - metabolism ; Transforming Growth Factor beta - immunology ; Tumor Necrosis Factor-alpha - immunology</subject><ispartof>Journal of autoimmunity, 2002-12, Vol.19 (4), p.169-174</ispartof><rights>2002 Elsevier Science Ltd</rights><rights>2003 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c439t-d74b9c70dde1e0fb917254f150774545e13547eba2f2381505eb3f2a7921da383</citedby><cites>FETCH-LOGICAL-c439t-d74b9c70dde1e0fb917254f150774545e13547eba2f2381505eb3f2a7921da383</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0896841102906189$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14376764$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12473237$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:1934543$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Duan, Rui-Sheng</creatorcontrib><creatorcontrib>Wang, Hua-Bing</creatorcontrib><creatorcontrib>Yang, Jian-She</creatorcontrib><creatorcontrib>Scallon, Bernie</creatorcontrib><creatorcontrib>Link, Hans</creatorcontrib><creatorcontrib>Xiao, Bao-Guo</creatorcontrib><title>Anti-TNF-α Antibodies Suppress the Development of Experimental Autoimmune Myasthenia Gravis</title><title>Journal of autoimmunity</title><addtitle>J Autoimmun</addtitle><description>To understand the role of TNF-α in the induction of experimental autoimmune myasthenia gravis (EAMG) and detect a possible effect of anti-TNF-α antibodies in the treatment of EAMG, anti-TNF-α antibodies were administrated intraperitoneally to Lewis rats twice per week for 5 weeks from the day of immunization with Torpedo AChR and complete Freund's adjuvant (CFA). Administration of anti-TNF-α antibodies resulted in lower incidence of EAMG, and in delayed onset and only mild muscle weakness compared with control EAMG rats. These mild clinical signs were accompanied by lower AChR-specific lymphocyte proliferation, down-regulated IFN-γ and IL-10, and up-regulated TGF-β. The lower levels of anti-AChR IgG, Ig2a and IgG2b and decreased anti-AChR IgG affinity were found in rats treated with anti-TNF-α antibodies. These results demonstrate that anti-TNF-α antibodies can suppress the induction and development of EAMG.</description><subject>Animals</subject><subject>Antibodies - immunology</subject><subject>Biological and medical sciences</subject><subject>Disease Models, Animal</subject><subject>Diseases of striated muscles. Neuromuscular diseases</subject><subject>Down-Regulation</subject><subject>experimental autoimmune myasthenia gravis, anti-TNF-α antibodies, cytokine, anti-AChR antibodies</subject><subject>Female</subject><subject>General aspects</subject><subject>Immunopathology</subject><subject>Interferon-gamma - immunology</subject><subject>Interleukin-10 - immunology</subject><subject>Medical sciences</subject><subject>Myasthenia Gravis, Autoimmune, Experimental - immunology</subject><subject>Myasthenia Gravis, Autoimmune, Experimental - prevention & control</subject><subject>Neurology</subject><subject>Rats</subject><subject>Rats, Inbred Lew</subject><subject>Receptors, Nicotinic - metabolism</subject><subject>T-Lymphocytes - immunology</subject><subject>Torpedo - metabolism</subject><subject>Transforming Growth Factor beta - immunology</subject><subject>Tumor Necrosis Factor-alpha - immunology</subject><issn>0896-8411</issn><issn>1095-9157</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc9u1DAQhy0EokvhyhHlArcsHv-J4-OqtAWppQfKDclynIlwSeJgJ9v2sXgRnqmJNmpPiJPHo8-j3_gj5C3QLVBafLyx07hllLItLaB8RjZAtcw1SPWcbGipi7wUAEfkVUo3lAJIKV-SI2BCccbVhvzY9aPPr7-e5X__ZEtdhdpjyr5NwxAxpWz8idkn3GMbhg77MQtNdno3YPTLzbbZbhqD77qpx-zy3qYZ773NzqPd-_SavGhsm_DNeh6T72en1yef84ur8y8nu4vcCa7HvFai0k7RukZA2lQaFJOiAUmVElJIBC6FwsqyhvFybkuseMOs0gxqy0t-TPLD3HSLw1SZYU5n470J1pu19Wuu0EgNhRAz_-HADzH8njCNpvPJYdvaHsOUjGJKCqb1f0EoCy5ALQm2B9DFkFLE5jEDULOIMosos4gyi6j5wbt18lR1WD_hq5kZeL8CNjnbNtH2zqcnTnBVqGLZpTxwOH_w3mM0yXnsHdY-ohtNHfy_MjwAurCv0g</recordid><startdate>20021201</startdate><enddate>20021201</enddate><creator>Duan, Rui-Sheng</creator><creator>Wang, Hua-Bing</creator><creator>Yang, Jian-She</creator><creator>Scallon, Bernie</creator><creator>Link, Hans</creator><creator>Xiao, Bao-Guo</creator><general>Elsevier Ltd</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>H94</scope><scope>7X8</scope><scope>ADTPV</scope><scope>AOWAS</scope></search><sort><creationdate>20021201</creationdate><title>Anti-TNF-α Antibodies Suppress the Development of Experimental Autoimmune Myasthenia Gravis</title><author>Duan, Rui-Sheng ; Wang, Hua-Bing ; Yang, Jian-She ; Scallon, Bernie ; Link, Hans ; Xiao, Bao-Guo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c439t-d74b9c70dde1e0fb917254f150774545e13547eba2f2381505eb3f2a7921da383</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Animals</topic><topic>Antibodies - immunology</topic><topic>Biological and medical sciences</topic><topic>Disease Models, Animal</topic><topic>Diseases of striated muscles. Neuromuscular diseases</topic><topic>Down-Regulation</topic><topic>experimental autoimmune myasthenia gravis, anti-TNF-α antibodies, cytokine, anti-AChR antibodies</topic><topic>Female</topic><topic>General aspects</topic><topic>Immunopathology</topic><topic>Interferon-gamma - immunology</topic><topic>Interleukin-10 - immunology</topic><topic>Medical sciences</topic><topic>Myasthenia Gravis, Autoimmune, Experimental - immunology</topic><topic>Myasthenia Gravis, Autoimmune, Experimental - prevention & control</topic><topic>Neurology</topic><topic>Rats</topic><topic>Rats, Inbred Lew</topic><topic>Receptors, Nicotinic - metabolism</topic><topic>T-Lymphocytes - immunology</topic><topic>Torpedo - metabolism</topic><topic>Transforming Growth Factor beta - immunology</topic><topic>Tumor Necrosis Factor-alpha - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Duan, Rui-Sheng</creatorcontrib><creatorcontrib>Wang, Hua-Bing</creatorcontrib><creatorcontrib>Yang, Jian-She</creatorcontrib><creatorcontrib>Scallon, Bernie</creatorcontrib><creatorcontrib>Link, Hans</creatorcontrib><creatorcontrib>Xiao, Bao-Guo</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><collection>SwePub</collection><collection>SwePub Articles</collection><jtitle>Journal of autoimmunity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Duan, Rui-Sheng</au><au>Wang, Hua-Bing</au><au>Yang, Jian-She</au><au>Scallon, Bernie</au><au>Link, Hans</au><au>Xiao, Bao-Guo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Anti-TNF-α Antibodies Suppress the Development of Experimental Autoimmune Myasthenia Gravis</atitle><jtitle>Journal of autoimmunity</jtitle><addtitle>J Autoimmun</addtitle><date>2002-12-01</date><risdate>2002</risdate><volume>19</volume><issue>4</issue><spage>169</spage><epage>174</epage><pages>169-174</pages><issn>0896-8411</issn><eissn>1095-9157</eissn><abstract>To understand the role of TNF-α in the induction of experimental autoimmune myasthenia gravis (EAMG) and detect a possible effect of anti-TNF-α antibodies in the treatment of EAMG, anti-TNF-α antibodies were administrated intraperitoneally to Lewis rats twice per week for 5 weeks from the day of immunization with Torpedo AChR and complete Freund's adjuvant (CFA). Administration of anti-TNF-α antibodies resulted in lower incidence of EAMG, and in delayed onset and only mild muscle weakness compared with control EAMG rats. These mild clinical signs were accompanied by lower AChR-specific lymphocyte proliferation, down-regulated IFN-γ and IL-10, and up-regulated TGF-β. The lower levels of anti-AChR IgG, Ig2a and IgG2b and decreased anti-AChR IgG affinity were found in rats treated with anti-TNF-α antibodies. These results demonstrate that anti-TNF-α antibodies can suppress the induction and development of EAMG.</abstract><cop>London</cop><pub>Elsevier Ltd</pub><pmid>12473237</pmid><doi>10.1006/jaut.2002.0618</doi><tpages>6</tpages></addata></record> |
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| subjects | Animals Antibodies - immunology Biological and medical sciences Disease Models, Animal Diseases of striated muscles. Neuromuscular diseases Down-Regulation experimental autoimmune myasthenia gravis, anti-TNF-α antibodies, cytokine, anti-AChR antibodies Female General aspects Immunopathology Interferon-gamma - immunology Interleukin-10 - immunology Medical sciences Myasthenia Gravis, Autoimmune, Experimental - immunology Myasthenia Gravis, Autoimmune, Experimental - prevention & control Neurology Rats Rats, Inbred Lew Receptors, Nicotinic - metabolism T-Lymphocytes - immunology Torpedo - metabolism Transforming Growth Factor beta - immunology Tumor Necrosis Factor-alpha - immunology |
| title | Anti-TNF-α Antibodies Suppress the Development of Experimental Autoimmune Myasthenia Gravis |
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