Upregulation of Macrophage Migration Inhibitory Factor (MIF) Production by Engagement of Toll-like Receptor 3 (TLR3) on Fibroblast-like Synoviocyte (FLS) from Patients with Rheumatoid Arthritis / 대한류마티스학회지
The Journal of the Korean Rheumatism Association
;
: 123-132, 2009.
Artigo
em Coreano
| WPRIM
| ID: wpr-83051
ABSTRACT
OBJECTIVE:
Rheumatoid arthritis (RA) is a chronic autoimmune disease. Macrophage migration inhibitory factor (MIF) has been shown to be an important pro-inflammatory cytokine in RA. The aim of this study was to determine if the engagement of toll-like receptor 3 (TLR3) induces the production of MIF in the fibroblast-like synoviocytes (FLS) of patients with RA.METHODS:
The expression of inflammatory cytokines (e.g. MIF, IL-6, IL-1beta and TNFalpha) and toll-like receptors (e.g. TLR2, TLR3 and TLR4) in the synovial tissue were quantified by immunohistochemistry. FLS were isolated from the synovial tissues of patients with RA and stimulated with TLR-3 ligand polyIC, in the presence of a neutralizing antibody against IL-6. The concentrations of MIF and IL-6 in the culture supernatants from the FLS were measured using sandwich ELISA.RESULTS:
The engagement of TLR3 with PolyIC increased the production of MIF in FLS. The stimulatory effect of these TLR ligands showed a dose-dependent trend. The combination of TLR3 and TLR4 synergistically increased the level of MIF and IL-6 production. The addition of neutralizing antibodies against IL-6 abrogated the stimulatory effect of the ligands of TLR3 and TLR4 on the production of MIF.CONCLUSION:
These results show that TLR3 engagement stimulates the production of MIF and IL-6. Therefore, the TLRs help perpetuate of RA pathogenesis through production of MIF from the FLS in patients with RA, and might provide a new therapeutic approach for the treatment of rheumatoid arthritis.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Artrite Reumatoide
/
Doenças Autoimunes
/
Ensaio de Imunoadsorção Enzimática
/
Imuno-Histoquímica
/
Regulação para Cima
/
Citocinas
/
Interleucina-6
/
Receptores Toll-Like
/
Receptor 3 Toll-Like
/
Anticorpos Neutralizantes
Limite:
Humanos
Idioma:
Coreano
Revista:
The Journal of the Korean Rheumatism Association
Ano de publicação:
2009
Tipo de documento:
Artigo
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