ABSENCE OF B7-DEPENDENT RESPONSES IN CD28-DEFICIENT MICE
ABSENCE OF B7-DEPENDENT RESPONSES IN CD28-DEFICIENT MICE
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DOI：
10.1016/1074-7613(94)90092-2
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发表时间：
1994-09-01
期刊：
影响因子：
32.4
通讯作者：
THOMPSON, CB
中科院分区：
文献类型：
--
作者：
GREEN, JM;NOEL, PJ;THOMPSON, CB
T细胞增殖的共刺激可以通过CD 28信号转导途径发生。此外，其他细胞表面受体，包括CD 28同源物CTLA-4，已被提出能够提供共刺激信号。我们研究了CD 28缺陷型T细胞对多种激动剂激活的反应。我们证明，在抗原呈递细胞或B7-1转染子的存在下，CD 28缺陷型T细胞的增殖显着减少。虽然CTLA-4可以在CD 28缺陷型T细胞上表达，但我们观察到在不存在CD 28的情况下没有B7依赖性共刺激。这些数据表明，CD 28是T细胞上主要的B7结合共刺激配体。此外，我们的数据表明，CD 28是主要的，也许是唯一的，共刺激受体所使用的传统抗原呈递细胞，以增加抗原活化的T细胞的增殖。
Costimulation of T cell proliferation can occur through the CD28 signal transduction pathway. In addition, other cell surface receptors, including the CD28 homolog CTLA-4, have been proposed to be capable of providing costimulatory signals. We have examined the response of CD28-deficient T cells to activation by a variety of agonists. We demonstrate that proliferation of CD28-deficient T cells in the presence of antigen-presenting cells or B7-1 transfectants is markedly reduced. Although CTLA-4 can be expressed on CD28-deficient T cells, we observed no B7-dependent costimulation in the absence of CD28. This data demonstrates that CD28 is the major B7-binding costimulatory ligand on T cells. Furthermore, our data suggest that CD28 is the primary, and perhaps exclusive, costimulatory receptor used by traditional antigen-presenting cells to augment the proliferation of antigen-activated T cells.