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Sayuri Yamazaki

Researcher at Nagoya City University

Publications -  47
Citations -  15056

Sayuri Yamazaki is an academic researcher from Nagoya City University. The author has contributed to research in topics: IL-2 receptor & FOXP3. The author has an hindex of 29, co-authored 45 publications receiving 14385 citations. Previous affiliations of Sayuri Yamazaki include Hokkaido University & Rockefeller University.

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Immunologic Self-Tolerance Maintained by Cd25+Cd4+Regulatory T Cells Constitutively Expressing Cytotoxic T Lymphocyte–Associated Antigen 4

TL;DR: Interference with this role of CTLA-4 suffices to elicit autoimmune disease in otherwise normal animals, presumably through affecting CD25+CD4+ T cell–mediated control of self-reactive T cells.
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Stimulation of CD25 + CD4 + regulatory T cells through GITR breaks immunological self-tolerance

TL;DR: GITR plays a key role in dominant immunological self-tolerance maintained by CD25+CD4+ regulatory T cells and could be a suitable molecular target for preventing or treating autoimmune disease.
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Immunologic tolerance maintained by CD25+ CD4+ regulatory T cells: their common role in controlling autoimmunity, tumor immunity, and transplantation tolerance.

TL;DR: There is accumulating evidence that T‐cell‐mediated dominant control of self‐reactive T‐cells contributes to the maintenance of immunologic self‐tolerance and its alteration can cause autoimmune disease.
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Induction of tumor immunity by removing CD25+CD4+ T cells: a common basis between tumor immunity and autoimmunity.

TL;DR: Removal of immunoregulatory CD25+4+ T cells can abrogate immunological unresponsiveness to syngeneic tumors in vivo and in vitro, leading to spontaneous development of tumor-specific effector cells as well as tumor-nonspecific ones.
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Differential antigen processing by dendritic cell subsets in vivo

TL;DR: This work targeted antigens to two major subsets of DCs by using chimeric monoclonal antibodies and found that this difference in antigen processing is intrinsic to the DC subsets and is associated with increased expression of proteins involved in MHC processing.