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Diabetes induced by Coxsackie virus: initiation by bystander damage and not molecular mimicry.
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- Additional Information
- Source:
Publisher: Nature Publishing Company Country of Publication: United States NLM ID: 9502015 Publication Model: Print Cited Medium: Print ISSN: 1078-8956 (Print) Linking ISSN: 10788956 NLM ISO Abbreviation: Nat Med Subsets: MEDLINE
- Publication Information:
Publication: New York Ny : Nature Publishing Company
Original Publication: New York, NY : Nature Pub. Co., [1995-
- Subject Terms:
Coxsackievirus Infections/
*immunology ;
Diabetes Mellitus, Type 1/
*immunology ;
Diabetes Mellitus, Type 1/
*virology ;
Enterovirus B, Human/
*immunology ;
Receptors, Antigen, T-Cell, alpha-beta/
*immunology ;
T-Lymphocytes/
*immunology;
Amino Acid Sequence ;
Animals ;
Cells, Cultured ;
Chaperonin 60/
immunology ;
Disease Models, Animal ;
Female ;
Glutamate Decarboxylase/
immunology ;
HeLa Cells ;
Humans ;
Hyaluronan Receptors/
immunology ;
L-Selectin/
immunology ;
Lymphocytic Choriomeningitis/
immunology ;
Mice ;
Mice, Inbred NOD ;
Mice, SCID ;
Mice, Transgenic ;
Molecular Sequence Data ;
Receptors, Antigen, T-Cell, alpha-beta/
genetics ;
Receptors, Interleukin-2/
immunology - 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.
- Comments:
Comment in: Nat Med. 1998 Jul;4(7):770-1. (PMID: 9662363)
- Accession Number:
0 (Chaperonin 60)
0 (Hyaluronan Receptors)
0 (Receptors, Antigen, T-Cell, alpha-beta)
0 (Receptors, Interleukin-2)
126880-86-2 (L-Selectin)
EC 4.1.1.15 (Glutamate Decarboxylase)
- Publication Date:
Date Created: 19980714 Date Completed: 19990407 Latest Revision: 20190914
- Publication Date:
20231215
- Accession Number:
10.1038/nm0798-781
- Accession Number:
9662368
No Comments.