CD28 COSTIMULATION CAN PROMOTE T-CELL SURVIVAL BY ENHANCING THE EXPRESSION OF BCL-X(L)
CD28 COSTIMULATION CAN PROMOTE T-CELL SURVIVAL BY ENHANCING THE EXPRESSION OF BCL-X(L)
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DOI：
10.1016/1074-7613(95)90161-2
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发表时间：
1995-07-01
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：
BOISE, LH;MINN, AJ;THOMPSON, CB
通过TCR的T细胞活化可导致细胞增殖或细胞死亡。共刺激受体在调节T细胞存活中的作用尚未确定。在这里，我们提出的数据表明，CD 28共刺激增强体外活化T细胞的存活。这种增强的一种机制是CD 28共刺激增加IL-2产生的能力，IL-2作为T细胞的外源性存活因子。此外，CD 28共刺激增强了T细胞抵抗凋亡的内在能力。虽然CD 28信号转导对Bcl-2表达没有影响，但发现CD 28共刺激显著增加Bcl-x（L）的表达。转染实验证明，这种水平的Bcl-x（L）可以防止响应于TCR交联、Fas交联或IL-2撤回的T细胞死亡。这些数据表明，CD 28共刺激的一个重要作用是在抗原活化过程中增加T细胞存活。
T cell activation through the TCR can result in either cell proliferation or cell death. The role of costimulatory receptors in regulating T cell survival has not been defined. Here, we present data demonstrating that CD28 costimulation enhances the in vitro survival of activated T cells. One mechanism for this enhancement is the ability of CD28 costimulation to augment the production of IL-2, which acts as an extrinsic survival factor for T cells. In addition, CD28 costimulation augments the intrinsic ability of T cells to resist apoptosis. Although CD28 signal transduction had no effect on Bcl-2 expression, CD28 costimulation was found to augment the expression of Bcl-x(L) substantially. Transfection experiments demonstrated that this level of Bcl-x(L) could prevent T cell death in response to TCR cross-linking, Fas cross-linking, or IL-2 withdrawal. These data suggest that an important role of CD28 costimulation is to augment T cell survival during antigen activation.