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Yoshiyuki Ohsugi

Researcher at Chugai Pharmaceutical Co.

Publications -  124
Citations -  7877

Yoshiyuki Ohsugi is an academic researcher from Chugai Pharmaceutical Co.. The author has contributed to research in topics: Antibody & Interleukin 6. The author has an hindex of 41, co-authored 124 publications receiving 7568 citations. Previous affiliations of Yoshiyuki Ohsugi include Osaka University & Shinshu University.

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Soluble interleukin-6 receptor triggers osteoclast formation by interleukin 6.

TL;DR: It is suggested that increased circulating or locally produced sIL-6R induces osteoclast formation in the presence of IL-6 mediated by a mechanism involving gp130, which may play an important physiological or pathological role in conditions associated with increased osteoclastic bone resorption.
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Reshaping a Human Antibody to Inhibit the Interleukin 6-dependent Tumor Cell Growth

TL;DR: The reshaped human PM-1 antibody, consisting of human REI-based light chain and NEW-based heavy chain variable regions, could be efficacious in human multiple myeloma patients.
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Soluble forms of the interleukin-6 signal-transducing receptor component gp130 in human serum possessing a potential to inhibit signals through membrane-anchored gp130

TL;DR: Results indicated that serum sgp130 could negatively regulate the IL-6 signal, implying physiologic roles of naturally produced serum s gp130 in modulating signals through gp130.
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IL-6 blockade inhibits the induction of myelin antigen-specific Th17 cells and Th1 cells in experimental autoimmune encephalomyelitis.

TL;DR: Findings indicate that anti-IL-6R mAb treatment might represent a novel therapy for human MS through the inhibition of the development of MOG-peptide-specific Th17 cells and Th1 cells, which in turn leads to reduced infiltration of T cells into the CNS.
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Tocilizumab inhibits signal transduction mediated by both mIL-6R and sIL-6R, but not by the receptors of other members of IL-6 cytokine family.

TL;DR: Significant lines of evidence indicate that tocilizumab is able to bind to both sIL-6R and mIL- 6R and to inhibit IL-6 binding to its receptors, leading to the blockade of the IL- 6 signaling through both sil-6r and mil-7R, but not block the signaling of other IL-7 family cytokines.