Deregulated T cell activation and autoimmunity in mice lacking interleukin-2 receptor beta.
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.
Pubmed ID: 7770771 RIS Download
Animals | Autoantibodies | Autoimmunity | B-Lymphocytes | CD4-Positive T-Lymphocytes | Female | Heterozygote | Homozygote | Lymph Nodes | Lymphocyte Activation | Male | Mice | Mice, Inbred C57BL | Mice, Nude | Mutagenesis, Insertional | Myeloproliferative Disorders | Receptors, Interleukin-2 | Signal Transduction | T-Lymphocytes | T-Lymphocytes, Cytotoxic