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Ji Hyeon Ju

Researcher at Catholic University of Korea

Publications -  226
Citations -  6319

Ji Hyeon Ju is an academic researcher from Catholic University of Korea. The author has contributed to research in topics: Arthritis & Induced pluripotent stem cell. The author has an hindex of 40, co-authored 212 publications receiving 5172 citations. Previous affiliations of Ji Hyeon Ju include Dongguk University & St Mary's Hospital.

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STAT3 and NF-κB Signal Pathway Is Required for IL-23-Mediated IL-17 Production in Spontaneous Arthritis Animal Model IL-1 Receptor Antagonist-Deficient Mice

TL;DR: The data suggest that IL-23 seems to be a central proinflammatory cytokine in the pathogenesis of this IL-1Ra−/− model of spontaneous arthritis, and its intracellular signaling pathway could be useful therapeutic targets in the treatment of autoimmune arthritis.
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Hyaluronate–Gold Nanoparticle/Tocilizumab Complex for the Treatment of Rheumatoid Arthritis

TL;DR: The therapeutic effect of HA-AuNP/TCZ complex on RA was confirmed in collagen-induced arthritis (CIA) model mice by ELISA, histological, and Western blot analyses.
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Human rheumatoid synovial fibroblasts promote osteoclastogenic activity by activating RANKL via TLR-2 and TLR-4 activation

TL;DR: The results suggest that the TLR signaling pathway, through TLR-2 andTLR-4, induces RANKL expression in RA-FLS and the expression of RankL promotes the differentiation of osteoclasts in RA synovium.
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IL-10 suppresses Th17 cells and promotes regulatory T cells in the CD4+ T cell population of rheumatoid arthritis patients

TL;DR: IT treatment significantly decreased the numbers of IL-17-producing and RORc-expressing cells among human CD4(+) T cells that had been activated in vitro by Th17-differentiating conditions in autoimmune arthritis patients.
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Up-regulation of stromal cell–derived factor 1 (CXCL12) production in rheumatoid synovial fibroblasts through interactions with T lymphocytes: Role of interleukin-17 and CD40L–CD40 interaction

TL;DR: SDF- 1 is overproduced in RA FLS, and IL-17 could up-regulate the expression of SDF-1 in RAFLS via pathways mediated by PI 3-kinase, NF-kappaB, and AP-1, and the findings suggest that inhibition of the interaction between T cells and SDF -1 in FLS may provide a new therapeutic approach in RA.