Methylation of CIITA promoter IV causes loss of HLA-II inducibility by IFN-γ in promyelocytic cells
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概要
- 論文の詳細を見る
- 2008-11-01
著者
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De Lerma
Department Of Clinical And Biological Sciences School Of Medicine University Of Insubria
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De Lerma
Department Of Clinical And Biological Sciences Unit Of General Pathology And Immunology School Of Me
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Accolla Roberto
Department Of Clinical And Biological Sciences School Of Medicine University Of Insubria
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Accolla Roberto
Department Of Clinical And Biological Sciences Unit Of General Pathology And Immunology School Of Me
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Romani Massimo
Laboratory Of Tumor Genetics Istituto Nazionale Per La Ricerca Sul Cancro (istituto Scientifico Tumo
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DE AMBROSIS
Laboratory of Traslational Pediatric Oncology, Istituto Nazionale per la Ricerca sul Cancro (Istitut
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BANELLI Barbara
Laboratory of Tumor Genetics, Istituto Nazionale per la Ricerca sul Cancro (Istituto Scientifico Tum
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PIRA Giuseppina
Laboratory of Cellular Immunology, Advanced Biotechnology Center
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ARESU Ottavia
Banca Biologica e Cell Factory, Istituto Nazionale per la Ricerca sul Cancro (IST)
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FERRINI Silvano
Laboratory of Immunological Therapy, Istitute Nazionale per la Ricerca sul Cancro (IST)
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Ferrini Silvano
Laboratory Of Immunological Therapy Istitute Nazionale Per La Ricerca Sul Cancro (ist)
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Banelli Barbara
Laboratory Of Tumor Genetics Istituto Nazionale Per La Ricerca Sul Cancro (istituto Scientifico Tumo
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De Ambrosis
Laboratory Of Traslational Pediatric Oncology Istituto Nazionale Per La Ricerca Sul Cancro (istituto
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Pira Giuseppina
Laboratory Of Cellular Immunology Advanced Biotechnology Center
関連論文
- Irradiated CIITA-positive mammary adenocarcinoma cells act as a potent anti-tumor-preventive vaccine by inducing tumor-specific CD4^+ T cell priming and CD8^+ T cell effector functions
- NK cells provide helper signal for CD8^+ T cells by inducing the expression of membrane-bound IL-15 on DCs
- Methylation of CIITA promoter IV causes loss of HLA-II inducibility by IFN-γ in promyelocytic cells
- Identification of new T_h peptides from the cytomegalovirus protein pp65 to design a peptide library for generation of CD4 T cell lines for cellular immunoreconstitution