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Altered expression of talin 1 in peripheral immune cells points to a significant role of the innate immune system in spontaneous autoimmune uveitis.
J. Proteomics 75, 4536-4544 (2012)
The molecular mechanism which enables activated immune cells to cross the blood-retinal barrier in spontaneous autoimmune uveitis is yet to be unraveled. Equine recurrent uveitis is the only spontaneous animal model allowing us to investigate the autoimmune mediated transformation of leukocytes in the course of this sight threatening disease. Hypothesizing that peripheral blood immune cells change their protein expression pattern in spontaneous autoimmune uveitis, we used DIGE to detect proteins with altered abundance comparing peripheral immune cells of healthy and ERU diseased horses. Among others, we found a significant downregulation of talin 1 in peripheral blood granulocytes of ERU specimen, pointing to changes in beta integrin activation and indicating a significant role of the innate immune system in spontaneous autoimmune diseases. This article is part of a Special Issue entitled: SI: Farm animal proteomics.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Immune Disease ; Dige ; Granulocytes ; Talin 1 ; Immunoproteomics ; Autoimmune; Equine Recurrent Uveitis; Multiple-Sclerosis; Integrin Activation; Dendritic Cells; Down-Regulation; Disease; Horses; Autoantigens; Binding; Domain
Language
english
Publication Year
2012
HGF-reported in Year
2012
ISSN (print) / ISBN
1874-3919
e-ISSN
1876-7737
Journal
Journal of Proteomics
Quellenangaben
Volume: 75,
Issue: 14,
Pages: 4536-4544
Publisher
Elsevier
Reviewing status
Peer reviewed
POF-Topic(s)
30203 - Molecular Targets and Therapies
30504 - Mechanisms of Genetic and Environmental Influences on Health and Disease
30504 - Mechanisms of Genetic and Environmental Influences on Health and Disease
Research field(s)
Enabling and Novel Technologies
Immune Response and Infection
Immune Response and Infection
PSP Element(s)
G-505700-001
G-501793-001
G-501793-001
PubMed ID
22306886
WOS ID
WOS:000307023900026
Scopus ID
84863834223
Erfassungsdatum
2012-09-21