| First Author | Suzuki H | Year | 1995 |
| Journal | Science | Volume | 268 |
| Issue | 5216 | Pages | 1472-6 |
| PubMed ID | 7770771 | Mgi Jnum | J:25940 |
| Mgi Id | MGI:73643 | Doi | 10.1126/science.7770771 |
| Citation | Suzuki H, et al. (1995) Deregulated T cell activation and autoimmunity in mice lacking interleukin-2 receptor beta. Science 268(5216):1472-6 |
| abstractText | In mice lacking the interleukin-2 receptor beta chain (IL-2R beta), T cells were shown to be spontaneously activated, resulting in exhaustive differentiation of B cells into plasma cells and the appearance of high serum concentrations of immunoglobulins G1 and E as well as autoantibodies that cause hemolytic anemia. Marked infiltrative granulocytopoiesis was also apparent, and the animals died after about 12 weeks. Depletion of CD4+ T cells in mutant mice rescued B cells without reversion of granulocyte abnormalities. T cells did not proliferate in response to polyclonal activators, nor could antigen-specific immune responses be elicited. Thus, IL-2R beta is required to keep the activation programs of T cells under control, to maintain homeostasis, and to prevent autoimmunity. |
