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首页> 外文期刊>Science >DEREGULATED T CELL ACTIVATION AND AUTOIMMUNITY IN MICE LACKING INTERLEUKIN-2 RECEPTOR BETA
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DEREGULATED T CELL ACTIVATION AND AUTOIMMUNITY IN MICE LACKING INTERLEUKIN-2 RECEPTOR BETA

机译:缺乏白细胞介素2受体β的小鼠中失调的T细胞活化和免疫原性

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摘要

In mice lacking the interleukin-2 receptor beta chain (lL-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.
机译:在缺乏白介素2受体β链(IL-2Rβ)的小鼠中,T细胞被证明是自发激活的,导致B细胞彻底分化为浆细胞,并出现了高血清浓度的免疫球蛋白G1和E作为导致溶血性贫血的自身抗体。明显的浸润性粒细胞减少也很明显,并且动物在约12周后死亡。突变小鼠中CD4(+)T细胞的耗竭挽救了B细胞,而没有粒细胞异常的逆转。 T细胞不会响应多克隆激活剂而增殖,也不会引起抗原特异性免疫反应。因此,需要IL-2R beta来保持T细胞的激活程序处于受控状态,以保持体内稳态,并防止自身免疫。

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