| Abstract: |
In this study, we describe the generation and characterization of mice in which GITR gene (TNFRSF18 [tumor necrosis factor receptor superfamily 18]), a member of the TNFRSF expressed mainly on T lymphocytes, has been ablated (GITR-/- mice). Results indicate that GITR inactivation does not impair the normal development of the lymphoid organs but modulates T-cell activation. In fact, when GITR-/- T lymphocytes are activated by treatment with an anti-CD3 monoclonal antibody they proliferate more than wild-type cells. Moreover, activated GITR-/- T lymphocytes express higher levels of interleukin-2 receptor, produce larger amounts of interleukin-2, and are more sensitive to activation-induced cell death than controls. These results suggest that GITR is involved in the regulation of T-cell receptor/CD3-driven T-cell activation and programmed cell death. © 2002 by The American Society of Hematology. |
| Keywords: |
controlled study; protein expression; unclassified drug; nonhuman; cell proliferation; t lymphocyte; antigens, cd3; t-lymphocytes; animal cell; mouse; animals; mice; mice, knockout; cell death; interleukin 2; apoptosis; monoclonal antibody; t lymphocyte receptor; lymphocyte activation; receptors, antigen, t-cell; adjuvants, immunologic; lymphoid organ; tumor necrosis factor; organogenesis; receptors, tumor necrosis factor; interleukin 2 receptor; receptors, nerve growth factor; priority journal; article; tumor necrosis factor gitr
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