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Shengdian Wang

Researcher at Chinese Academy of Sciences

Publications -  67
Citations -  5661

Shengdian Wang is an academic researcher from Chinese Academy of Sciences. The author has contributed to research in topics: T cell & Cytotoxic T cell. The author has an hindex of 30, co-authored 64 publications receiving 4954 citations. Previous affiliations of Shengdian Wang include Johns Hopkins University & Mayo Clinic.

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Journal Article

Blockade of B7-H1 and PD-1 by Monoclonal Antibodies Potentiates Cancer Therapeutic Immunity

TL;DR: It is reported here that constitutive or inducible expression of B7-H1, a B7 family molecule widely expressed by cancers, confers resistance to therapeutic anti-CD137 antibody in mice with established tumors and implicate new approaches for immunotherapy of human cancers.
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B7-H4, a molecule of the B7 family, negatively regulates T cell immunity.

TL;DR: A B7 family molecule, B7-H4, is identified by protein sequence analysis and comparative molecular modeling and may participate in negative regulation of cell-mediated immunity in peripheral tissues.
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The Therapeutic Effect of Anti-HER2/neu Antibody Depends on Both Innate and Adaptive Immunity

TL;DR: It is demonstrated that the mechanisms of tumor regression by anti-HER2/neu antibody therapy also require the adaptive immune response, and the addition of chemotherapeutic drugs, although capable of enhancing the reduction of tumor burden, could abrogate antibody-initiated immunity leading to decreased resistance to rechallenge or earlier relapse.
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Costimulation of T cells by B7-H2, a B7-like molecule that binds ICOS

TL;DR: The results indicate that B7-H2 is a putative ligand for the ICOS T-cell molecule.
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Molecular Modeling and Functional Mapping of B7-H1 and B7-DC Uncouple Costimulatory Function from PD-1 Interaction

TL;DR: This work finds that nonconserved residues between these ligands on the A′GFCC′C′′ face mediate interaction with PD-1, indicating significant structural heterogeneity of the interactions between PD-2 and its ligands and providing direct evidence for an independent costimulatory receptor other than PD- 1.