Alteration of a polyclonal to an oligoclonal immune response to cecal aerobic bacterial antigens in TCRα mutant mice with inflammatory bowel disease
スポンサーリンク
概要
著者
-
MIZOGUCHI Atsushi
Experimental Pathology, Massachusetts General Hospital
-
Bhan Atul
Experimental Pathology Massachusetts General Hospital
-
TONEGAWA Susumu
Howard Hughes Medical Institute at Center for Cancer Research and Department of Biology Massachusett
-
Tonegawa Susumu
Howard Hughes Medical Institute Center For Cancer Research And Department Of Biology
-
Mizoguchi Emiko
Department Of Pathology Harvard Medical School
-
MIZOGUCHI Atsushi
The Immunopathology Unit, Department of Pathology, Massachusetts General Hospital, Harvard Medical S
-
MIZOGUCHI Emiko
The Immunopathology Unit, Department of Pathology, Massachusetts General Hospital, Harvard Medical S
-
BHAN Atul
The Immunopathology Unit, Department of Pathology, Massachusetts General Hospital, Harvard Medical S
-
Mizoguchi Atsushi
Experimental Pathology Massachusetts General Hospital
関連論文
- Regulatory role of B-1 B cells in chronic colitis
- Rearrangement and expression of Vγ1, Vγ2 and Vγ3 TCR γ genes in C57BL/6 mice
- Alpha beta and gamma delta T cells in the immune response to the erythrocytic stages of malaria in mice
- MHC class 1 expression and CD8+ T cell development in TAP1/beta2-microglobulin double mutant mice
- Alteration of a polyclonal to an oligoclonal immune response to cecal aerobic bacterial antigens in TCRα mutant mice with inflammatory bowel disease
- Role of the CD5 molecule on TCR γδ T cell-mediated immune functions: development of germinal centers and chronic intestinal inflammation
- Blocking inducible co-stimulator in the absence of CD28 impairs T_h1 and CD25^+ regulatory T cells in murine colitis
- Essential role for Vav1 in activation, but not development, of γδ T cells
- Regulatory role of mature B cells in a murine model of inflammatory bowel disease
- Impaired B cell maturation in mice lacking Bruton's tyrosine kinase (Btk) and CD40
- Double-positive thymocytes resistant to antigen-MHC-induced negative selection lack active caspase