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Haruo Tsuchiya

Researcher at Johns Hopkins University

Publications -  13
Citations -  2677

Haruo Tsuchiya is an academic researcher from Johns Hopkins University. The author has contributed to research in topics: T cell & Dendritic cell. The author has an hindex of 9, co-authored 13 publications receiving 2534 citations. Previous affiliations of Haruo Tsuchiya include Johns Hopkins University School of Medicine & Mayo Clinic.

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Expression of Programmed Death 1 Ligands by Murine T Cells and APC

TL;DR: B7-H1 was broadly expressed on the surface of mouse tumor cell lines while the expression of B7-DC was rather restricted, and the inducible expression of PD-1 ligands on both T cells and APCs may suggest new paradigms ofPD-1-mediated immune regulation.
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B7-Dc, a New Dendritic Cell Molecule with Potent Costimulatory Properties for T Cells

TL;DR: A new B7 family member, B7-DC, whose expression is highly restricted to DCs, was identified among a library of genes differentially expressed between DCs and activated macrophages, which may account for some of the unique activity of DC's, such as their ability to initiate potent T helper cell type 1 responses.
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Cutting edge: Expression of functional CD137 receptor by dendritic cells.

TL;DR: It is reported that freshly isolated mouse splenic DCs and bone marrow-derived DCs express CD137 on the cell surface and in soluble form, and infusion of an agonistic mAb to CD137 into naive mice enhanced the ability of DCs to stimulate T cell proliferation in response to both alloantigens and a nominal Ag in vitro.
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Cooperative B7-1/2 (CD80/CD86) and B7-DC Costimulation of CD4+ T Cells Independent of the PD-1 Receptor

TL;DR: DCs from B7-DC KO mice are diminished in their ability to activate CD4+ T cells, demonstrating that DC-expressed B 7-DC serves a predominantly stimulatory rather than inhibitory function in the initiation of T cell responses.
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In vivo costimulatory role of B7-DC in tuning T helper cell 1 and cytotoxic T lymphocyte responses

TL;DR: It is indicated that B7-DC functions as a tuning molecule, selectively augmenting T helper 1 and CTL responses, and is associated with a decrease in intrahepatic tumor-specific CD8 T cells.