Citations |
Ko, K., Yamazaki, S., Nakamura, K., Nishioka, T., Hirota, K., Yamaguchi, T., ... & Sakaguchi, S. (2005). Treatment of advanced tumors with agonistic anti-GITR mAb and its effects on tumor-infiltrating Foxp3+ CD25+ CD4+ regulatory T cells. The Journal of experimental medicine, 202(7), 885-891. Shimizu, J., Yamazaki, S., Takahashi, T., Ishida, Y., & Sakaguchi, S. (2002). Stimulation of CD25+ CD4+ regulatory T cells through GITR breaks immunological self-tolerance. Nature immunology, 3(2), 135-142. Tone, M., Tone, Y., Adams, E., Yates, S. F., Frewin, M. R., Cobbold, S. P., & Waldmann, H. (2003). Mouse glucocorticoid-induced tumor necrosis factor receptor ligand is costimulatory for T cells. Proceedings of the National Academy of Sciences, 100(25), 15059-15064. |
Description |
The DTA-1 monoclonal antibody specifically reacts with mouse Glucocorticoid-Induced TNFR-related protein, also known as GITR and TNFRSF18, a 66-70 kDa homodimer glycoprotein, detected in the T cells treated with glucocorticoid dexamethasone. GITR is also expressed in naive mice by CD25+/CD4+/CD8a- thymocytes and on CD25+/CD4+/CD45RB-low splenocytes. Low levels were detected in splenic CD25+/CD4+/CD45RB-low T cells, B cells, dendritic cells and macrophages. A GITR ligand was detected on dendritic cells, macrophages and B cells.The DTA-1 antibody stimulates GITR and abrogates suppression by T regulatory cells (Treg), without affecting their proliferation. DTA-1 administration or the removal of GITR-expressing cells led to organ specific autoimmune disease. |