How viral infections enhance or prevent type 1 diabetes-from mouse to man

More recent evidence shows that viral infections can enhance as well as prevent type 1 diabetes in experimental animal models [Filippi and von Herrath, 2010]. Published findings clearly indicate that the replication levels of the virus [Tracy et al., 2010] as well as the timing of infection [Richer...

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Vydané v:	Journal of medical virology Ročník 83; číslo 9; s. 1672
Hlavní autori:	von Herrath, M., Filippi, C., Coppieters, K.
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	Hoboken Wiley Subscription Services, Inc., A Wiley Company 01.09.2011 Wiley Subscription Services, Inc
Predmet:	Animals Diabetes Mellitus, Type 1 - prevention & control Diabetes Mellitus, Type 1 - virology Enterovirus Enterovirus Infections Genes, MHC Class I Humans Islets of Langerhans - virology Mice Mice, Inbred NOD Prevalence Toll-Like Receptor 2 Virology
ISSN:	0146-6615, 1096-9071, 1096-9071
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Abstract	More recent evidence shows that viral infections can enhance as well as prevent type 1 diabetes in experimental animal models [Filippi and von Herrath, 2010]. Published findings clearly indicate that the replication levels of the virus [Tracy et al., 2010] as well as the timing of infection [Richer and Horwitz, 2009] in relation to the autoimmune process both play an instrumental role. For example, enteroviruses replicating to higher levels, accelerate type 1 diabetes, whereas lower replication rates result in the prevention of diabetes. In human pancreata, elevated levels of MHC class 1 were detected in many islets which could be an indicator of a persistent infection. When present, the increased MHC affected all islet cells. MHC upregulation was present in a lobular and patchy fashion, and in many but not all cases associated with CD8 infiltration. In vivo tetramer staining showed that many of these CD8s cells were specific for beta cell antigens. It is proposed that it is possible that a persistent viral infection could unmask human islets for recognition by autoreactive CD8 T cells [von Herrath, 2009]. Indeed in animal models upregulation of MHC class 1 on beta cells is a pre‐requisite for their destruction. On the other hand, prevention of diabetes in NOD mice by Coxsackie viruses was associated with “invigorated” Tregs that was present in higher numbers and produced more TGF‐beta [Filippi et al., 2009]. This phenomenon was TLR‐2 dependent and effects of TLR‐2 on TLR as well as on dendritic cells was a contributory factor. Therefore antiviral vaccines targeting for example enteroviruses might be able to influence the prevalence of human diabetes. J. Med. Virol. 83:1672–1672, 2011. © 2011 Wiley‐Liss, Inc.
AbstractList	More recent evidence shows that viral infections can enhance as well as prevent type 1 diabetes in experimental animal models [Filippi and von Herrath, 2010 ]. Published findings clearly indicate that the replication levels of the virus [Tracy et al., 2010 ] as well as the timing of infection [Richer and Horwitz, 2009 ] in relation to the autoimmune process both play an instrumental role. For example, enteroviruses replicating to higher levels, accelerate type 1 diabetes, whereas lower replication rates result in the prevention of diabetes. In human pancreata, elevated levels of MHC class 1 were detected in many islets which could be an indicator of a persistent infection. When present, the increased MHC affected all islet cells. MHC upregulation was present in a lobular and patchy fashion, and in many but not all cases associated with CD8 infiltration. In vivo tetramer staining showed that many of these CD8s cells were specific for beta cell antigens. It is proposed that it is possible that a persistent viral infection could unmask human islets for recognition by autoreactive CD8 T cells [von Herrath, 2009 ]. Indeed in animal models upregulation of MHC class 1 on beta cells is a pre-requisite for their destruction. On the other hand, prevention of diabetes in NOD mice by Coxsackie viruses was associated with "invigorated" Tregs that was present in higher numbers and produced more TGF-beta [Filippi et al., 2009 ]. This phenomenon was TLR-2 dependent and effects of TLR-2 on TLR as well as on dendritic cells was a contributory factor. Therefore antiviral vaccines targeting for example enteroviruses might be able to influence the prevalence of human diabetes. J. Med. Virol. 83:1672-1672, 2011. copyright 2011 Wiley-Liss, Inc. More recent evidence shows that viral infections can enhance as well as prevent type 1 diabetes in experimental animal models [Filippi and von Herrath, 2010]. Published findings clearly indicate that the replication levels of the virus [Tracy et al., 2010] as well as the timing of infection [Richer and Horwitz, 2009] in relation to the autoimmune process both play an instrumental role. For example, enteroviruses replicating to higher levels, accelerate type 1 diabetes, whereas lower replication rates result in the prevention of diabetes. In human pancreata, elevated levels of MHC class 1 were detected in many islets which could be an indicator of a persistent infection. When present, the increased MHC affected all islet cells. MHC upregulation was present in a lobular and patchy fashion, and in many but not all cases associated with CD8 infiltration. In vivo tetramer staining showed that many of these CD8s cells were specific for beta cell antigens. It is proposed that it is possible that a persistent viral infection could unmask human islets for recognition by autoreactive CD8 T cells [von Herrath, 2009]. Indeed in animal models upregulation of MHC class 1 on beta cells is a pre‐requisite for their destruction. On the other hand, prevention of diabetes in NOD mice by Coxsackie viruses was associated with “invigorated” Tregs that was present in higher numbers and produced more TGF‐beta [Filippi et al., 2009]. This phenomenon was TLR‐2 dependent and effects of TLR‐2 on TLR as well as on dendritic cells was a contributory factor. Therefore antiviral vaccines targeting for example enteroviruses might be able to influence the prevalence of human diabetes. J. Med. Virol. 83:1672–1672, 2011. © 2011 Wiley‐Liss, Inc. More recent evidence shows that viral infections can enhance as well as prevent type 1 diabetes in experimental animal models [Filippi and von Herrath, 2010 ]. Published findings clearly indicate that the replication levels of the virus [Tracy et al., 2010 ] as well as the timing of infection [Richer and Horwitz, 2009 ] in relation to the autoimmune process both play an instrumental role. For example, enteroviruses replicating to higher levels, accelerate type 1 diabetes, whereas lower replication rates result in the prevention of diabetes. In human pancreata, elevated levels of MHC class 1 were detected in many islets which could be an indicator of a persistent infection. When present, the increased MHC affected all islet cells. MHC upregulation was present in a lobular and patchy fashion, and in many but not all cases associated with CD8 infiltration. In vivo tetramer staining showed that many of these CD8s cells were specific for beta cell antigens. It is proposed that it is possible that a persistent viral infection could unmask human islets for recognition by autoreactive CD8 T cells [von Herrath, 2009 ]. Indeed in animal models upregulation of MHC class 1 on beta cells is a pre‐requisite for their destruction. On the other hand, prevention of diabetes in NOD mice by Coxsackie viruses was associated with “invigorated” Tregs that was present in higher numbers and produced more TGF‐beta [Filippi et al., 2009 ]. This phenomenon was TLR‐2 dependent and effects of TLR‐2 on TLR as well as on dendritic cells was a contributory factor. Therefore antiviral vaccines targeting for example enteroviruses might be able to influence the prevalence of human diabetes. J. Med. Virol. 83:1672–1672, 2011. © 2011 Wiley‐Liss, Inc. More recent evidence shows that viral infections can enhance as well as prevent type 1 diabetes in experimental animal models [Filippi and von Herrath, 2010]. Published findings clearly indicate that the replication levels of the virus [Tracy et al., 2010] as well as the timing of infection [Richer and Horwitz, 2009] in relation to the autoimmune process both play an instrumental role. For example, enteroviruses replicating to higher levels, accelerate type 1 diabetes, whereas lower replication rates result in the prevention of diabetes. In human pancreata, elevated levels of MHC class 1 were detected in many islets which could be an indicator of a persistent infection. When present, the increased MHC affected all islet cells. MHC upregulation was present in a lobular and patchy fashion, and in many but not all cases associated with CD8 infiltration. In vivo tetramer staining showed that many of these CD8s cells were specific for beta cell antigens. It is proposed that it is possible that a persistent viral infection could unmask human islets for recognition by autoreactive CD8 T cells [von Herrath, 2009]. Indeed in animal models upregulation of MHC class 1 on beta cells is a pre-requisite for their destruction. On the other hand, prevention of diabetes in NOD mice by Coxsackie viruses was associated with "invigorated" Tregs that was present in higher numbers and produced more TGF-beta [Filippi et al., 2009]. This phenomenon was TLR-2 dependent and effects of TLR-2 on TLR as well as on dendritic cells was a contributory factor. Therefore antiviral vaccines targeting for example enteroviruses might be able to influence the prevalence of human diabetes. J. Med. Virol. 83:1672-1672, 2011. © 2011 Wiley-Liss, Inc. [PUBLICATION ABSTRACT]
Author	von Herrath, M. Coppieters, K. Filippi, C.
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Cites_doi	10.1111/j.1749-6632.2009.04662.x 10.1038/459518a 10.1002/rmv.639 10.1111/j.1365-2249.2010.04128.x
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References_xml	– reference: von Herrath MG. 2009. Diabetes: A virus-gene collaboration. Nature 459: 518-519. – reference: Tracy S, Drescher KM, Jackson JD, Kim K, Kono K. 2010. Enteroviruses, type 1 diabetes and hygiene: A complex relationship. Rev Med Virol 20: 106-116. – reference: Filippi CM, von Herrath MG. 2010. 99th Dahlem conference on infection, inflammation and chronic inflammatory disorders: Viruses, autoimmunity and immunoregulation. Clin Exp Immunol 160: 113-119. – reference: Filippi CM, Estes EA, Oldham JG, von Herrath MG. 2009. Immunoregulatory mechanisms triggered by virus infections protect from type 1 diabetes in mice. J Clin Invest 119: 1515-1523. – reference: Richer MJ, Horwitz MS. 2009. Preventig viral-induced type 1 diabetes. Ann N Y Acad Sci 1173: 487-492. – volume: 119 start-page: 1515 year: 2009 end-page: 1523 article-title: Immunoregulatory mechanisms triggered by virus infections protect from type 1 diabetes in mice publication-title: J Clin Invest – volume: 459 start-page: 518 year: 2009 end-page: 519 article-title: Diabetes: A virus‐gene collaboration publication-title: Nature – volume: 20 start-page: 106 year: 2010 end-page: 116 article-title: Enteroviruses, type 1 diabetes and hygiene: A complex relationship publication-title: Rev Med Virol – volume: 1173 start-page: 487 year: 2009 end-page: 492 article-title: Preventig viral‐induced type 1 diabetes publication-title: Ann N Y Acad Sci – volume: 160 start-page: 113 year: 2010 end-page: 119 article-title: 99th Dahlem conference on infection, inflammation and chronic inflammatory disorders: Viruses, autoimmunity and immunoregulation publication-title: Clin Exp Immunol – ident: e_1_2_1_4_1 doi: 10.1111/j.1749-6632.2009.04662.x – ident: e_1_2_1_6_1 doi: 10.1038/459518a – ident: e_1_2_1_5_1 doi: 10.1002/rmv.639 – ident: e_1_2_1_2_1 doi: 10.1111/j.1365-2249.2010.04128.x – volume: 119 start-page: 1515 year: 2009 ident: e_1_2_1_3_1 article-title: Immunoregulatory mechanisms triggered by virus infections protect from type 1 diabetes in mice publication-title: J Clin Invest
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SubjectTerms	Animals Diabetes Mellitus, Type 1 - prevention & control Diabetes Mellitus, Type 1 - virology Enterovirus Enterovirus Infections Genes, MHC Class I Humans Islets of Langerhans - virology Mice Mice, Inbred NOD Prevalence Toll-Like Receptor 2 Virology
Title	How viral infections enhance or prevent type 1 diabetes-from mouse to man
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