Diabetes induced by Coxsackie virus: Initiation by bystander damage and not molecular mimicry
Viral induction of autoimmunity is thought to occur by either bystander T-cell activation or molecular mimicry. Coxsackie B4 virus is strongly associated with the development of insulin-dependent diabetes mellitus in humans and shares sequence similarity with the islet autoantigen glutamic acid deca...
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| Veröffentlicht in: | Nature medicine 1998-07, Vol.4 (7), p.781-785 |
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| creator | Horwitz, Marc S Bradley, Linda M Harbertson, Judith Krahl, Troy Lee, Jae Sarvennick, Nora |
| description | Viral induction of autoimmunity is thought to occur by either bystander T-cell activation or molecular mimicry. Coxsackie B4 virus is strongly associated with the development of insulin-dependent diabetes mellitus in humans and shares sequence similarity with the islet autoantigen glutamic acid decarboxylase. We infected different strains of mice with Coxsackie B4 virus to discriminate between the two possible induction mechanisms, and found that mice with susceptible MHC alleles had no viral acceleration of diabetes, but mice with a T cell receptor transgene specific for a different islet autoantigen rapidly developed diabetes. These results show that diabetes induced by Coxsackie virus infection is a direct result of local infection leading to inflammation, tissue damage, and the release of sequestered islet antigen resulting in the re-stimulation of resting autoreactive T cells, further indicating that the islet antigen sensitization is an indirect consequence of the viral infection. |
| doi_str_mv | 10.1038/nm0798-781 |
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Coxsackie B4 virus is strongly associated with the development of insulin-dependent diabetes mellitus in humans and shares sequence similarity with the islet autoantigen glutamic acid decarboxylase. We infected different strains of mice with Coxsackie B4 virus to discriminate between the two possible induction mechanisms, and found that mice with susceptible MHC alleles had no viral acceleration of diabetes, but mice with a T cell receptor transgene specific for a different islet autoantigen rapidly developed diabetes. These results show that diabetes induced by Coxsackie virus infection is a direct result of local infection leading to inflammation, tissue damage, and the release of sequestered islet antigen resulting in the re-stimulation of resting autoreactive T cells, further indicating that the islet antigen sensitization is an indirect consequence of the viral infection.</description><identifier>ISSN: 1078-8956</identifier><identifier>EISSN: 1546-170X</identifier><identifier>DOI: 10.1038/nm0798-781</identifier><identifier>PMID: 9662368</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>Amino Acid Sequence ; Animals ; Biomedical and Life Sciences ; Biomedicine ; Cancer Research ; Cells, Cultured ; Chaperonin 60 - immunology ; Coxsackievirus Infections - immunology ; Diabetes Mellitus, Type 1 - immunology ; Diabetes Mellitus, Type 1 - virology ; Disease Models, Animal ; Enterovirus B, Human - immunology ; Female ; Glutamate Decarboxylase - immunology ; HeLa Cells ; Humans ; Hyaluronan Receptors - immunology ; Infectious Diseases ; L-Selectin - immunology ; Lymphocytic Choriomeningitis - immunology ; Metabolic Diseases ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Mice, Transgenic ; Molecular Medicine ; Molecular Sequence Data ; Neurosciences ; Receptors, Antigen, T-Cell, alpha-beta - genetics ; Receptors, Antigen, T-Cell, alpha-beta - immunology ; Receptors, Interleukin-2 - immunology ; T-Lymphocytes - immunology</subject><ispartof>Nature medicine, 1998-07, Vol.4 (7), p.781-785</ispartof><rights>Springer Nature America, Inc. 1998</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c374t-ce8d01727a7b70fb381c0c15fc3724f6125a70071dea5cae92207b762302c69d3</citedby><cites>FETCH-LOGICAL-c374t-ce8d01727a7b70fb381c0c15fc3724f6125a70071dea5cae92207b762302c69d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/nm0798-781$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/nm0798-781$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,778,782,27911,27912,41475,42544,51306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9662368$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Horwitz, Marc S</creatorcontrib><creatorcontrib>Bradley, Linda M</creatorcontrib><creatorcontrib>Harbertson, Judith</creatorcontrib><creatorcontrib>Krahl, Troy</creatorcontrib><creatorcontrib>Lee, Jae</creatorcontrib><creatorcontrib>Sarvennick, Nora</creatorcontrib><title>Diabetes induced by Coxsackie virus: Initiation by bystander damage and not molecular mimicry</title><title>Nature medicine</title><addtitle>Nat Med</addtitle><addtitle>Nat Med</addtitle><description>Viral induction of autoimmunity is thought to occur by either bystander T-cell activation or molecular mimicry. Coxsackie B4 virus is strongly associated with the development of insulin-dependent diabetes mellitus in humans and shares sequence similarity with the islet autoantigen glutamic acid decarboxylase. We infected different strains of mice with Coxsackie B4 virus to discriminate between the two possible induction mechanisms, and found that mice with susceptible MHC alleles had no viral acceleration of diabetes, but mice with a T cell receptor transgene specific for a different islet autoantigen rapidly developed diabetes. These results show that diabetes induced by Coxsackie virus infection is a direct result of local infection leading to inflammation, tissue damage, and the release of sequestered islet antigen resulting in the re-stimulation of resting autoreactive T cells, further indicating that the islet antigen sensitization is an indirect consequence of the viral infection.</description><subject>Amino Acid Sequence</subject><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>Cells, Cultured</subject><subject>Chaperonin 60 - immunology</subject><subject>Coxsackievirus Infections - immunology</subject><subject>Diabetes Mellitus, Type 1 - immunology</subject><subject>Diabetes Mellitus, Type 1 - virology</subject><subject>Disease Models, Animal</subject><subject>Enterovirus B, Human - immunology</subject><subject>Female</subject><subject>Glutamate Decarboxylase - immunology</subject><subject>HeLa Cells</subject><subject>Humans</subject><subject>Hyaluronan Receptors - immunology</subject><subject>Infectious Diseases</subject><subject>L-Selectin - immunology</subject><subject>Lymphocytic Choriomeningitis - immunology</subject><subject>Metabolic Diseases</subject><subject>Mice</subject><subject>Mice, Inbred NOD</subject><subject>Mice, SCID</subject><subject>Mice, Transgenic</subject><subject>Molecular Medicine</subject><subject>Molecular Sequence Data</subject><subject>Neurosciences</subject><subject>Receptors, Antigen, T-Cell, alpha-beta - genetics</subject><subject>Receptors, Antigen, T-Cell, alpha-beta - immunology</subject><subject>Receptors, Interleukin-2 - immunology</subject><subject>T-Lymphocytes - immunology</subject><issn>1078-8956</issn><issn>1546-170X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1LxDAQhoMouq5evAs5eVCqk3abD2-yfi0IXhS8SEnTqUTbVJNW3H9vpMt6ETxlwvvwwjxDyAGDUwaZPHMtCCUTIdkGmbB8xhMm4GkzziBkIlXOd8huCK8AkEGutsm24jzNuJyQ50urS-wxUOuqwWBFyyWdd19BmzeL9NP6IZzThbO91b3t3E9cLkOvXYWeVrrVL0jjh7qup23XoBka7WlrW2v8co9s1boJuL96p-Tx-uphfpvc3d8s5hd3icnErE8MygqYSIUWpYC6zCQzYFhexzid1ZyluRYAglWoc6NRpSlEMq4AqeGqyqbkaOx9993HgKEvWhsMNo122A2hEEopyTPxL8h4ziRPWQSPR9D4LgSPdfHubav9smBQ_EgvRulFlB7hw1XrULZYrdGV5ZifjHmIiXtBX7x2g3fRyN9tdKSd7geP67bfK2ffXJKVxg</recordid><startdate>199807</startdate><enddate>199807</enddate><creator>Horwitz, Marc S</creator><creator>Bradley, Linda M</creator><creator>Harbertson, Judith</creator><creator>Krahl, Troy</creator><creator>Lee, Jae</creator><creator>Sarvennick, Nora</creator><general>Nature Publishing Group US</general><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>7U9</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>199807</creationdate><title>Diabetes induced by Coxsackie virus: Initiation by bystander damage and not molecular mimicry</title><author>Horwitz, Marc S ; Bradley, Linda M ; Harbertson, Judith ; Krahl, Troy ; Lee, Jae ; Sarvennick, Nora</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c374t-ce8d01727a7b70fb381c0c15fc3724f6125a70071dea5cae92207b762302c69d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Amino Acid Sequence</topic><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cancer Research</topic><topic>Cells, Cultured</topic><topic>Chaperonin 60 - immunology</topic><topic>Coxsackievirus Infections - immunology</topic><topic>Diabetes Mellitus, Type 1 - immunology</topic><topic>Diabetes Mellitus, Type 1 - virology</topic><topic>Disease Models, Animal</topic><topic>Enterovirus B, Human - immunology</topic><topic>Female</topic><topic>Glutamate Decarboxylase - immunology</topic><topic>HeLa Cells</topic><topic>Humans</topic><topic>Hyaluronan Receptors - immunology</topic><topic>Infectious Diseases</topic><topic>L-Selectin - immunology</topic><topic>Lymphocytic Choriomeningitis - immunology</topic><topic>Metabolic Diseases</topic><topic>Mice</topic><topic>Mice, Inbred NOD</topic><topic>Mice, SCID</topic><topic>Mice, Transgenic</topic><topic>Molecular Medicine</topic><topic>Molecular Sequence Data</topic><topic>Neurosciences</topic><topic>Receptors, Antigen, T-Cell, alpha-beta - genetics</topic><topic>Receptors, Antigen, T-Cell, alpha-beta - immunology</topic><topic>Receptors, Interleukin-2 - immunology</topic><topic>T-Lymphocytes - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Horwitz, Marc S</creatorcontrib><creatorcontrib>Bradley, Linda M</creatorcontrib><creatorcontrib>Harbertson, Judith</creatorcontrib><creatorcontrib>Krahl, Troy</creatorcontrib><creatorcontrib>Lee, Jae</creatorcontrib><creatorcontrib>Sarvennick, Nora</creatorcontrib><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>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Nature medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Horwitz, Marc S</au><au>Bradley, Linda M</au><au>Harbertson, Judith</au><au>Krahl, Troy</au><au>Lee, Jae</au><au>Sarvennick, Nora</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Diabetes induced by Coxsackie virus: Initiation by bystander damage and not molecular mimicry</atitle><jtitle>Nature medicine</jtitle><stitle>Nat Med</stitle><addtitle>Nat Med</addtitle><date>1998-07</date><risdate>1998</risdate><volume>4</volume><issue>7</issue><spage>781</spage><epage>785</epage><pages>781-785</pages><issn>1078-8956</issn><eissn>1546-170X</eissn><abstract>Viral induction of autoimmunity is thought to occur by either bystander T-cell activation or molecular mimicry. Coxsackie B4 virus is strongly associated with the development of insulin-dependent diabetes mellitus in humans and shares sequence similarity with the islet autoantigen glutamic acid decarboxylase. We infected different strains of mice with Coxsackie B4 virus to discriminate between the two possible induction mechanisms, and found that mice with susceptible MHC alleles had no viral acceleration of diabetes, but mice with a T cell receptor transgene specific for a different islet autoantigen rapidly developed diabetes. These results show that diabetes induced by Coxsackie virus infection is a direct result of local infection leading to inflammation, tissue damage, and the release of sequestered islet antigen resulting in the re-stimulation of resting autoreactive T cells, further indicating that the islet antigen sensitization is an indirect consequence of the viral infection.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>9662368</pmid><doi>10.1038/nm0798-781</doi><tpages>5</tpages></addata></record> |
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| source | MEDLINE; Nature; Springer Nature - Complete Springer Journals |
| subjects | Amino Acid Sequence Animals Biomedical and Life Sciences Biomedicine Cancer Research Cells, Cultured Chaperonin 60 - immunology Coxsackievirus Infections - immunology Diabetes Mellitus, Type 1 - immunology Diabetes Mellitus, Type 1 - virology Disease Models, Animal Enterovirus B, Human - immunology Female Glutamate Decarboxylase - immunology HeLa Cells Humans Hyaluronan Receptors - immunology Infectious Diseases L-Selectin - immunology Lymphocytic Choriomeningitis - immunology Metabolic Diseases Mice Mice, Inbred NOD Mice, SCID Mice, Transgenic Molecular Medicine Molecular Sequence Data Neurosciences Receptors, Antigen, T-Cell, alpha-beta - genetics Receptors, Antigen, T-Cell, alpha-beta - immunology Receptors, Interleukin-2 - immunology T-Lymphocytes - immunology |
| title | Diabetes induced by Coxsackie virus: Initiation by bystander damage and not molecular mimicry |
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