Document Detail


Expression level of a pancreatic neo-antigen in beta cells determines degree of diabetes pathogenesis.
MedLine Citation:
PMID:  20932718     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
It is not fully understood how the expression level of autoantigens in beta cells impacts autoimmune diabetes (T1D) development. Earlier studies using ovalbumin and also insulin had shown that secreted antigens could enhance diabetes development through facilitated presentation by antigen presenting cells. Here we sought to determine how the expression level of a membrane bound, non-secreted or cross-presented neo-antigen, the glycoprotein (GP) of lymphocytic choriomeningitis virus (LCMV), would influence T1D. We found that an RIP-LCMV transgenic mouse line exhibiting higher levels of beta cell GP expression developed more severe diabetes after LCMV infection or transfer of high numbers of activated autoreactive T cells. Importantly, all beta cells were lost and a significant increase in morbidity and mortality from T1D was noted. Insulitis and accumulation of autoaggressive CD8 cells was more profound in the RIP-LCMV-GP high-expressor line. Interestingly, the additional introduction of neo-antigen-specific CD4(+) helper or regulatory T cells was able to influence diabetogenesis positively or negatively. We conclude that a higher degree of autoantigen expression results in increased diabetes susceptibility. Therefore, autoantigens such as insulin that are expressed at higher levels in beta cells might have a more profound impact on diabetes pathogenesis.
Authors:
Marianne M Martinic; Christoph Huber; Ken Coppieters; Janine E Oldham; Amanda L Gavin; Matthias G von Herrath
Related Documents :
3902008 - Anomeric specificity of hexokinase and glucokinase activities in liver and insulin-prod...
14720288 - Bioartificial pancreas research in japan.
16447058 - Gamma-aminobutyric acid up- and downregulates insulin secretion from beta cells in conc...
7420058 - Regulation of synthesis of beta-fructofuranosidase (invertase) in streptococcus mitis.
21033698 - Improvement of insulin resistance by removal of systemic hydrogen peroxide by pegylated...
3902008 - Anomeric specificity of hexokinase and glucokinase activities in liver and insulin-prod...
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2010-10-06
Journal Detail:
Title:  Journal of autoimmunity     Volume:  35     ISSN:  1095-9157     ISO Abbreviation:  J. Autoimmun.     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2010-10-25     Completed Date:  2011-05-23     Revised Date:  2011-12-21    
Medline Journal Info:
Nlm Unique ID:  8812164     Medline TA:  J Autoimmun     Country:  England    
Other Details:
Languages:  eng     Pagination:  404-13     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Elsevier Ltd. All rights reserved.
Affiliation:
Type 1 Diabetes Center at the La Jolla Institute for Allergy & Immunology, La Jolla, CA 92037, USA. mariannemartinic@yahoo.de
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Adoptive Transfer
Animals
Antigens, Viral / biosynthesis,  genetics
Arenaviridae Infections / genetics,  immunology*,  physiopathology
Autoantigens / biosynthesis,  genetics
CD8-Positive T-Lymphocytes / immunology,  metabolism*,  pathology,  transplantation
Cells, Cultured
Cross-Priming / genetics
Cytotoxicity, Immunologic / genetics
Diabetes Mellitus, Type 1 / genetics,  immunology*,  physiopathology
Disease Progression
Glycoproteins / biosynthesis,  genetics
Insulin-Secreting Cells / metabolism*,  pathology
Lymphocyte Activation / genetics
Lymphocytic choriomeningitis virus / pathogenicity,  physiology*
Mice
Mice, Transgenic
Receptors, Antigen, T-Cell / genetics
Grant Support
ID/Acronym/Agency:
A1067403//PHS HHS; DK78013/DK/NIDDK NIH HHS; P01 AI058105-01/AI/NIAID NIH HHS; P01 AI058105-010001/AI/NIAID NIH HHS; P01 AI058105-02/AI/NIAID NIH HHS; P01 AI058105-020001/AI/NIAID NIH HHS; P01 AI058105-03/AI/NIAID NIH HHS; P01 AI058105-030001/AI/NIAID NIH HHS; P01 AI058105-04/AI/NIAID NIH HHS; P01 AI058105-040001/AI/NIAID NIH HHS; P01 AI058105-05/AI/NIAID NIH HHS; P01 AI058105-050001/AI/NIAID NIH HHS; P01 AI058105-05S1/AI/NIAID NIH HHS; P01 AI058105-05S10001/AI/NIAID NIH HHS; P01 AI58105/AI/NIAID NIH HHS; R01 AI067403-01A2/AI/NIAID NIH HHS; R01 AI067403-02/AI/NIAID NIH HHS; R01 AI067403-03/AI/NIAID NIH HHS
Chemical
Reg. No./Substance:
0/Antigens, Viral; 0/Autoantigens; 0/Glycoproteins; 0/Receptors, Antigen, T-Cell

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Gaussian mixtures on tensor fields for segmentation: Applications to medical imaging.
Next Document:  CXCL10 promotes liver fibrosis by prevention of NK cell mediated hepatic stellate cell inactivation.