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Mol Med Rep. 2014 Mar;9(3):899-903. doi: 10.3892/mmr.2014.1893. Epub 2014 Jan 13.

Local delivery of T-bet shRNA reduces inflammation in collagen II-induced arthritis via downregulation of IFN-γ and IL-17.

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Department of Immunology, Institute of Laboratory Medicine, Jiangsu University, Zhenjiang, Jiangsu 212013, P.R. China.
The Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu 212001, P.R. China.


Th1 and Th17 cells are involved in the pathogenesis of rheumatoid arthritis (RA). T-bet, a Th1-specific transcription factor, appears to drive the maturation of Th1 and IFN-γ secretion. In the present study, we established the T-bet shRNA recombinant plasmid (p-T-shRNA) and explored its possible anti-inflammatory effect in a collagen-induced arthritis (CIA) model by local injection of plasmid vectors. For the initiation of CIA, DBA/1J mice were immunized with type II collagen (CII) in Freund's adjuvant and the CII-immunized mice were treated with p-T-shRNA. Levels of T-bet, IFN-γ, IL-17 and RORγt mRNA in splenocytes and synovial joints were measured by quantitative real-time PCR and T-bet expression in joint tissue was detected by immunohistochemistry staining. The intracellular IFN-γ and IL-17 were analyzed by flow cytometry (FCM). The results demonstrated that therapeutic administration on the local joints with p-T-shRNA significantly suppressed IFN-γ and IL-17 gene expression and improved the pathogenesis of arthritis in CIA mice, while administration of a plasmid expressing T-bet (pIRES-T-bet) accelerated the disease onset. Our study suggests that T-bet may be developed as a potential target for arthritis therapy.

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