Chamoto K | Division Of Immunoregulation Section Of Disease Control Institute For Genetic Medicine And Hokkaido

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著作論文

CpG-ODN inhibits airway inflammation at effector phase through down-regulation of antigen-specific T_h2-cell migration into lung
Anti-OX40 monoclonal antibody therapy in combination with radiotherapy results in therapeutic antitumor immunity to murine lung cancer
Tetramer-blocking assay for defining antigen-specific cytotoxic T lymphocytes using peptide-MHC tetramer
An indispensable role of type-1 IFNs for inducing CTL-mediated complete eradication of established tumor tissue by CpG-liposome co-encapsulated with model tumor antigen
STAT6-mediated signaling in Th2-dependent allergic asthma : critical role for the development of eosinophilia, airway hyper-responsiveness and mucus hypersecretion, distinct from its role in Th2 differentiation
The critical role of type-1 innate and acquired immunity in tumor immunotherapy
3-Methylcholanthrene-induced transforming growth factor-β-producing carcinomas, but not sarcomas, are refractory to regulatory T cell-depletion therapy
Critical role of the Th1/Tc1 circuit for the generation of tumor-specific CTL during tumor eradication in vivo by Th1-cell therapy
Combination immunotherapy with radiation and CpG-based tumor vaccination for the eradication of radio- and immuno-resistant lung carcinoma cells
Unexpected role of TNF-α in graft versus host reaction (GVHR) : donor-derived TNF-α suppresses GVHR via inhibition of IFN-γ-dependent donor type-1 immunity
Differential regulation of VLA-2 expression on T_h1 and T_2 cells : a novel marker for the classification of T_h subsets
An efficient method to prepare T cell receptor gene-transduced cytotoxic T lymphocytes type 1 applicable to tumor gene cell-therapy
Blocking of IL-6 signaling pathway prevents CD4^+ T cell-mediated colitis in a T_h17-independent manner
Th1 cell adjuvant therapy combined with tumor vaccination: a novel strategy for promoting CTL responses while avoiding the accumulation of Tregs.
A T_h17-polarized cell population that has infiltrated the lung requires cells that convert to IFN-γ production in order to induce airway hyperresponsiveness

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