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Hiromitsu Kimura

Researcher at Tokyo Medical and Dental University

Publications -  38
Citations -  1023

Hiromitsu Kimura is an academic researcher from Tokyo Medical and Dental University. The author has contributed to research in topics: Transplantation & Antigen. The author has an hindex of 14, co-authored 38 publications receiving 988 citations. Previous affiliations of Hiromitsu Kimura include National Institutes of Health.

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Amelioration of Experimental Autoimmune Encephalomyelitis in Lewis Rats by FTY720 Treatment

TL;DR: The results suggested that the protective anti-inflammatory effect of treatment with FTY720 was, to a large extent, due to the inhibition of encephalitogenic T-cell responses and/or their migration into the central nervous system and may be a potential candidate for use in treating patients with MS.
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Amelioration of experimental autoimmune encephalomyelitis by curcumin treatment through inhibition of IL-17 production.

TL;DR: Results indicated that curcumin amelioration EAE was, to a large extent, due to inhibit differentiation and development of Th17 cells depends on down-regulating expression of IL-6, IL-21, RORgammat signaling and inhibition STAT3-phosphorylation, suggests it is useful in the treatment of MS and other Th17 cell-mediated inflammatory diseases.
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Involvement of the programmed death-1/programmed death-1 ligand pathway in CD4+CD25+ regulatory T-cell activity to suppress alloimmune responses

TL;DR: The blockade of the PD-1/PD-L1 pathway abrogates Treg-mediated immunoregulation, thus suggesting that thePD-1 /PD- L1 pathway is required for Treg suppression of the alloreactive responses of CD4+CD25-T cells.
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Prolonged survival in rat liver transplantation with mouse monoclonal antibody against an inducible costimulator (ICOS).

TL;DR: T-cell activation through the ICOS costimulatory pathway plays an important role in graft rejection, and manipulating its pathway is an effective method for modulating transplantation immunity.
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Superagonist CD28 antibody preferentially expanded Foxp3-expressing nTreg cells and prevented graft-versus-host diseases.

TL;DR: It is shown that naturally occurring CD4+CD25+ Treg cells preferentially proliferate to a fourfold increase within 3 days in response to the administration of a single superagonistic CD28-specific monoclonal antibody (supCD28 mAb).