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Mi La Cho

Researcher at Catholic University of Korea

Publications -  95
Citations -  2923

Mi La Cho is an academic researcher from Catholic University of Korea. The author has contributed to research in topics: Medicine & Arthritis. The author has an hindex of 30, co-authored 60 publications receiving 2648 citations. Previous affiliations of Mi La Cho include Dongguk University.

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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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Type II collagen autoimmunity in a mouse model of human rheumatoid arthritis.

TL;DR: The available information on anti-CII immunity is summarized and recent updates regarding pathogenesis in the CIA model are discussed, including the role of Th17 cells.
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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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Elevated vascular endothelial growth factor in systemic sclerosis.

TL;DR: The extent of skin sclerosis may contribute to the elevation of serum VEGf and high VEGF levels may serve as a surrogate indicator of capillary damage in SSc, and no significant differences were found in the serum levels of V EGF between patients with systemic organ involvement and those without.
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CD40 engagement on synovial fibroblast up-regulates production of vascular endothelial growth factor

TL;DR: Results suggest that the interaction between CD40 on synovial fibroblasts and CD40L expressed on activated T lymphocytes may be directly involved in the neovascularization in rheumatoid synovitis by enhancing the production of VEGF.