Resistance of MHC Class I-Deficient Mice to Experimental Systemic Lupus Erythematosus
Experimental systemic lupus erythematosus (SLE) can be induced in mice by immunization with a human monoclonal antibody to DNA that bears a common idiotype (16/6Id). These mice generate antibodies to 16/6Id, antibodies to DNA, and antibodies directed against nuclear antigens. Subsequently, manifesta...
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Veröffentlicht in: | Science (American Association for the Advancement of Science) 1993-07, Vol.261 (5117), p.91-93 |
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creator | Mozes, Edna Kohn, Leonard D. Hakim, Fran Singer, Dinah S. |
description | Experimental systemic lupus erythematosus (SLE) can be induced in mice by immunization with a human monoclonal antibody to DNA that bears a common idiotype (16/6Id). These mice generate antibodies to 16/6Id, antibodies to DNA, and antibodies directed against nuclear antigens. Subsequently, manifestations of SLE develop, including leukopenia, proteinuria, and immune complex deposits in the kidney. In contrast, after immunization with 16/6Id, mice lacking major histocompatibility complex (MHC) class I molecules generated antibodies to 16/6Id but did not generate antibodies to DNA or to nuclear antigen. Furthermore, they did not develop any of the above clinical manifestations. These results reveal an unexpected function of MHC class I in the induction of autoimmune SLE. |
doi_str_mv | 10.1126/science.8316860 |
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These mice generate antibodies to 16/6Id, antibodies to DNA, and antibodies directed against nuclear antigens. Subsequently, manifestations of SLE develop, including leukopenia, proteinuria, and immune complex deposits in the kidney. In contrast, after immunization with 16/6Id, mice lacking major histocompatibility complex (MHC) class I molecules generated antibodies to 16/6Id but did not generate antibodies to DNA or to nuclear antigen. Furthermore, they did not develop any of the above clinical manifestations. These results reveal an unexpected function of MHC class I in the induction of autoimmune SLE.</description><identifier>ISSN: 0036-8075</identifier><identifier>EISSN: 1095-9203</identifier><identifier>DOI: 10.1126/science.8316860</identifier><identifier>PMID: 8316860</identifier><identifier>CODEN: SCIEAS</identifier><language>eng</language><publisher>Washington, DC: American Society for the Advancement of Science</publisher><subject>Animals ; Antibodies ; Antibodies, Antinuclear - immunology ; Antibodies, Monoclonal - immunology ; Antigens ; Biological and medical sciences ; DNA ; Experimental and animal immunopathology. 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These mice generate antibodies to 16/6Id, antibodies to DNA, and antibodies directed against nuclear antigens. Subsequently, manifestations of SLE develop, including leukopenia, proteinuria, and immune complex deposits in the kidney. In contrast, after immunization with 16/6Id, mice lacking major histocompatibility complex (MHC) class I molecules generated antibodies to 16/6Id but did not generate antibodies to DNA or to nuclear antigen. Furthermore, they did not develop any of the above clinical manifestations. These results reveal an unexpected function of MHC class I in the induction of autoimmune SLE.</description><subject>Animals</subject><subject>Antibodies</subject><subject>Antibodies, Antinuclear - immunology</subject><subject>Antibodies, Monoclonal - immunology</subject><subject>Antigens</subject><subject>Biological and medical sciences</subject><subject>DNA</subject><subject>Experimental and animal immunopathology. Animal models</subject><subject>Histocompatibility Antigens Class I - immunology</subject><subject>Immunity, Innate</subject><subject>Immunization</subject><subject>Immunoglobulin Idiotypes - immunology</subject><subject>Immunopathology</subject><subject>Kidneys</subject><subject>Lupus Erythematosus, Systemic - immunology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Nuclear antigens</subject><subject>Systemic lupus erythematosus</subject><subject>T lymphocytes</subject><subject>Titration</subject><issn>0036-8075</issn><issn>1095-9203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkMFLwzAUh4MoOqdnLwo5iLe6pEnT9ChzOmFDUHcuafqClXadfSm4_96MlXn0lEe-7_1CfoRccXbPeawmaCtYW7jXgiut2BEZcZYlURYzcUxGjAkVaZYmZ-Qc8YuxwDJxSk4HfURWb4AVehMyaOvocj6l09og0pfoEVy1S_d0WQXqWzr72UBXNeHK1PR9ix6aytJFv-mRzrqt_4TG-BZ7vCAnztQIl8M5Jqun2cd0Hi1en1-mD4vISqV9JEpXpIUGqyHj1pWs1MC5TkCGscgUOMgSKxyXpZRFYlOQVsnM2LhQwlkpxuRun7vp2u8e0OdNhRbq2qyh7TFPE80US9W_IldKapGxIE72ou1axA5cvgk_Nt025yzfNZ4PjedDhWHjZojuiwbKg__Hbwdu0JradaHrCg9aeJapJA3a9V77Qt92BxxrzWUai18EQJSW</recordid><startdate>19930702</startdate><enddate>19930702</enddate><creator>Mozes, Edna</creator><creator>Kohn, Leonard D.</creator><creator>Hakim, Fran</creator><creator>Singer, Dinah S.</creator><general>American Society for the Advancement of Science</general><general>American Association for the Advancement of Science</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></search><sort><creationdate>19930702</creationdate><title>Resistance of MHC Class I-Deficient Mice to Experimental Systemic Lupus Erythematosus</title><author>Mozes, Edna ; Kohn, Leonard D. ; Hakim, Fran ; Singer, Dinah S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c468t-3dfb7b8ec8e91cfd0d8e1185e4d0db96efe95c3f14d44b5c7e4c649ac2b63fc43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Animals</topic><topic>Antibodies</topic><topic>Antibodies, Antinuclear - immunology</topic><topic>Antibodies, Monoclonal - immunology</topic><topic>Antigens</topic><topic>Biological and medical sciences</topic><topic>DNA</topic><topic>Experimental and animal immunopathology. Animal models</topic><topic>Histocompatibility Antigens Class I - immunology</topic><topic>Immunity, Innate</topic><topic>Immunization</topic><topic>Immunoglobulin Idiotypes - immunology</topic><topic>Immunopathology</topic><topic>Kidneys</topic><topic>Lupus Erythematosus, Systemic - immunology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Nuclear antigens</topic><topic>Systemic lupus erythematosus</topic><topic>T lymphocytes</topic><topic>Titration</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mozes, Edna</creatorcontrib><creatorcontrib>Kohn, Leonard D.</creatorcontrib><creatorcontrib>Hakim, Fran</creatorcontrib><creatorcontrib>Singer, Dinah S.</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><jtitle>Science (American Association for the Advancement of Science)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mozes, Edna</au><au>Kohn, Leonard D.</au><au>Hakim, Fran</au><au>Singer, Dinah S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Resistance of MHC Class I-Deficient Mice to Experimental Systemic Lupus Erythematosus</atitle><jtitle>Science (American Association for the Advancement of Science)</jtitle><addtitle>Science</addtitle><date>1993-07-02</date><risdate>1993</risdate><volume>261</volume><issue>5117</issue><spage>91</spage><epage>93</epage><pages>91-93</pages><issn>0036-8075</issn><eissn>1095-9203</eissn><coden>SCIEAS</coden><abstract>Experimental systemic lupus erythematosus (SLE) can be induced in mice by immunization with a human monoclonal antibody to DNA that bears a common idiotype (16/6Id). These mice generate antibodies to 16/6Id, antibodies to DNA, and antibodies directed against nuclear antigens. Subsequently, manifestations of SLE develop, including leukopenia, proteinuria, and immune complex deposits in the kidney. In contrast, after immunization with 16/6Id, mice lacking major histocompatibility complex (MHC) class I molecules generated antibodies to 16/6Id but did not generate antibodies to DNA or to nuclear antigen. Furthermore, they did not develop any of the above clinical manifestations. These results reveal an unexpected function of MHC class I in the induction of autoimmune SLE.</abstract><cop>Washington, DC</cop><pub>American Society for the Advancement of Science</pub><pmid>8316860</pmid><doi>10.1126/science.8316860</doi><tpages>3</tpages></addata></record> |
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subjects | Animals Antibodies Antibodies, Antinuclear - immunology Antibodies, Monoclonal - immunology Antigens Biological and medical sciences DNA Experimental and animal immunopathology. Animal models Histocompatibility Antigens Class I - immunology Immunity, Innate Immunization Immunoglobulin Idiotypes - immunology Immunopathology Kidneys Lupus Erythematosus, Systemic - immunology Medical sciences Mice Nuclear antigens Systemic lupus erythematosus T lymphocytes Titration |
title | Resistance of MHC Class I-Deficient Mice to Experimental Systemic Lupus Erythematosus |
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