T cell sensitivity to TGF-β is required for the effector function but not the generation of splenic CD8^+ regulatory T cells induced via the injection of antigen into the anterior chamber
スポンサーリンク
概要
- 論文の詳細を見る
- 2009-05-01
著者
-
CONE Robert
Department of Immunology, University of Connecticut Health Center
-
CHATTOPADHYAY Subhasis
Department of Immunology, University of Connecticut Health Center
-
SHARAFIEH Roshanak
Department of Immunology, University of Connecticut Health Center
-
LEMIRE Yen
Department of Immunology, University of Connecticut Health Center
-
FLAVELL Richard
Department of Immunobiology and Howard Hughes Medical Institute, Yale University School of Medicine
-
CLARK Robert
Department of Immunology, University of Connecticut Health Center
-
O'rourke James
Department Of Immunology University Of Connecticut Health Center
-
Lemire Yen
Department Of Immunology University Of Connecticut Health Center
-
Cone Robert
Department Of Immunology University Of Connecticut Health Center
-
Clark Robert
Department Of Immunology University Of Connecticut Health Center
-
Sharafieh Roshanak
Department Of Immunology University Of Connecticut Health Center
-
Chattopadhyay Subhasis
Department Of Immunology University Of Connecticut Health Center
-
Flavell Richard
Department Of Immunobiology And Howard Hughes Medical Institute Yale University School Of Medicine
関連論文
- T cell sensitivity to TGF-β is required for the effector function but not the generation of splenic CD8^+ regulatory T cells induced via the injection of antigen into the anterior chamber
- Polyl : C-induced reduction in uptake of soluble antigen is independent of dendritic cell activation
- Implication for the CD94/NKG2A-Qa-1 system in the generation and function of ocular-induced splenic CD8^+ regulatory T cells
- The generation of encephalitogenic T cell lines form experimental allergic encephalomyelitis-resistant strains of mice
- Mechanisums of immune tolerance induction through the thymic expression of a peripheral tissue-specific protein
- A crucial role of CD4 T cells as a functional source of CD154 in the initiation of insulin-dependent diabetes mellitus in the non-obese diabetic mouse