Abstract:
:Functional analysis of single Toll-like receptors (TLRs) in vivo is necessary to understand how they shape the ocular inflammation involved in uveitis. In this study we explored the role and mechanisms of TLR-2 agonists on the autoreactive T helper type 17 (Th17) response in experimental autoimmune uveitis (EAU). Treatment by peptidoglycan (PGN), a specific TLR-2 agonist, remarkably increased mRNA levels of Th17-lineage genes interleukin (IL)-17A, IL-21 and RAR-related orphan receptor (ROR)γt and promoted antigen-specific Th17 response in EAU mice. A mixture of PGN and interphotoreceptor retinoid-binding protein peptide (IRBP161-180 ) could effectively induce EAU in the absence of complete Freund's adjuvant (CFA). PGN treatment also enhanced the pathogenic activities of activated antigen-specific Th17 cells in vivo. PGN significantly increased the production of IL-1β, IL-6 and IL-23 of dendritic cells (DCs) and enhanced their ability to promote IL-17(+) uveitogenic T cells. Enhanced immunostimulatory activities of PGN-DCs depend upon p38 activation. Inhibition of p38 mitogen-activated protein kinase (MAPK) activity dramatically decreased IL-17 gene expression and antigen-specific Th17 responses stimulated by PGN-DCs. Our findings suggest that PGN treatment dramatically promotes the IL-17(+) uveitogenic T cell responses via enhancing the immunostimulatory activities of DCs. This effect may be mediated, at least in part, by activation of the p38 signalling pathway in DCs.
journal_name
Clin Exp Immunoljournal_title
Clinical and experimental immunologyauthors
Wei R,Dong L,Xiao Q,Sun D,Li X,Nian Hdoi
10.1111/cei.12405subject
Has Abstractpub_date
2014-11-01 00:00:00pages
353-63issue
2eissn
0009-9104issn
1365-2249journal_volume
178pub_type
杂志文章abstract::Interstitial mononuclear cell infiltration in rats during the development of autoimmune Heymann nephritis (HN) was studied using the fine-needle aspiration biopsy (FNAB) technique. The results were compared with those obtained by immunohistochemical studies of infiltrating T helper (T-h) and T suppressor/cytotoxic (T-...
journal_title:Clinical and experimental immunology
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doi:
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journal_title:Clinical and experimental immunology
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journal_title:Clinical and experimental immunology
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journal_title:Clinical and experimental immunology
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journal_title:Clinical and experimental immunology
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journal_title:Clinical and experimental immunology
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doi:
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journal_title:Clinical and experimental immunology
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journal_title:Clinical and experimental immunology
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journal_title:Clinical and experimental immunology
pub_type: 杂志文章
doi:
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journal_title:Clinical and experimental immunology
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doi:
更新日期:1986-01-01 00:00:00
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journal_title:Clinical and experimental immunology
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doi:
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journal_title:Clinical and experimental immunology
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doi:
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journal_title:Clinical and experimental immunology
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journal_title:Clinical and experimental immunology
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journal_title:Clinical and experimental immunology
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journal_title:Clinical and experimental immunology
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journal_title:Clinical and experimental immunology
pub_type: 杂志文章
doi:
更新日期:1984-09-01 00:00:00
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journal_title:Clinical and experimental immunology
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doi:
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journal_title:Clinical and experimental immunology
pub_type: 杂志文章
doi:
更新日期:1984-07-01 00:00:00