Modulation of CD4 co-receptor limits spontaneous autoimmunity when high-affinity transgenic TCR specific for self-antigen is expressed on a genetically resistant background
スポンサーリンク
概要
- 論文の詳細を見る
- 2007-10-01
著者
-
Kuchroo Vijay
Center For Neurologic Diseases Brigham And Women's Hospital Harvard Medical School
-
Kuchroo Vijay
Center For Neurologic Diseases Harvard Institute Of Medicine Brigham And Women's Hospital Harva
-
Reddy Jayagopala
Center For Neurologic Diseases Brigham And Women's Hospital Harvard Medical School
-
Sobel Raymond
Laboratory Service Veterans Affairs Medical Center
-
ILLES Zsolt
Center for Neurologic Diseases, Harvard Institute of Medicine, Brigham and Women's Hospital, Harvard
-
WALDNER Hanspeter
Center for Neurologic Diseases, Harvard Institute of Medicine, Brigham and Women's Hospital, Harvard
-
ANDERSON Ana
Center for Neurologic Diseases, Harvard Institute of Medicine, Brigham and Women's Hospital, Harvard
-
Illes Zsolt
Center For Neurologic Diseases Harvard Institute Of Medicine Brigham And Women's Hospital Harva
-
Anderson Ana
Center For Neurologic Diseases Harvard Institute Of Medicine Brigham And Women's Hospital Harva
-
Reddy Jayagopala
Center For Neurologic Diseases Harvard Institute Of Medicine Brigham And Women's Hospital Harva
-
Waldner Hanspeter
Center For Neurologic Diseases Harvard Institute Of Medicine Brigham And Women's Hospital Harva
関連論文
- IL-2-induced tumor necrosis factor (TNF)-β expression : further analysis in the IL-2 knockout model, and comparison with TNF-α, lymphotoxin-β, TNFR1 and TNFR2 modulation
- Recovery from experimental allergic encephalomyelitis is TGF-β dependent and associated with increases in CD4^+LAP^+ and CD4^+CD25^+ T cells
- IL-10 is involved in the suppression of experimental autoimmune encephalomyelitis by CD25^+ CD4^+ regulatory T cells
- Genetic susceptibility or resistance to autoimmune encephalomyelitis in MHC congenic mice is associated with differential production of pro- and anti-inflammatory
- Modulation of CD4 co-receptor limits spontaneous autoimmunity when high-affinity transgenic TCR specific for self-antigen is expressed on a genetically resistant background
- Changes in the strength of co-stimulation through the B7/CD28 pathway alter functional T cell responses to altered peptide ligands
- Tuning T cell activation threshold and effector function with cross-reactive peptide ligands
- A chimeric T cell receptor with super-signaling properties
- T_h17 cells : from precursors to players in inflammation and infection