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Yoshimasa Tanaka

Researcher at Nagasaki University

Publications -  218
Citations -  15690

Yoshimasa Tanaka is an academic researcher from Nagasaki University. The author has contributed to research in topics: T cell & Antigen. The author has an hindex of 44, co-authored 194 publications receiving 13756 citations. Previous affiliations of Yoshimasa Tanaka include Hyogo College of Medicine & Panasonic.

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Involvement of PD-L1 on tumor cells in the escape from host immune system and tumor immunotherapy by PD-L1 blockade

TL;DR: The results suggest that the expression of PD-L1 can serve as a potent mechanism for potentially immunogenic tumors to escape from host immune responses and that blockade of interaction between PD-1 andPD-L may provide a promising strategy for specific tumor immunotherapy.
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Autoimmune Dilated Cardiomyopathy in PD-1 Receptor-Deficient Mice

TL;DR: Results indicate that PD-1 may be an important factor contributing to the prevention of autoimmune diseases and high-titer circulating IgG autoantibodies reactive to a 33-kilodalton protein expressed specifically on the surface of cardiomyocytes.
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Programmed cell death 1 ligand 1 and tumor-infiltrating CD8+ T lymphocytes are prognostic factors of human ovarian cancer.

TL;DR: Multivariate analysis showed the expression of PD-L1 on tumor cells and intraepithelial CD8+ T lymphocyte count are independent prognostic factors and the PD-1/PD-L pathway can be a good target for restoring antitumor immunity in ovarian cancer.
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Natural and synthetic non-peptide antigens recognized by human γδ T cells

TL;DR: Results provide formal evidence that, in contrast to recognition of major histocompatibility complex-bound peptide antigens by αβ T cells, human γδ T cells can recognize naturally occurring small non-peptidic antIGens.
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Risk Factors Contributing to Type 2 Diabetes and Recent Advances in the Treatment and Prevention

TL;DR: The core aims are to bring forward the new therapy strategies and cost-effective intervention trials of type 2 diabetes, and the roles of genes, lifestyle and other factors contributing to rapid increase in the incidence of type 1 diabetes.