Antigen-specific T cell activation results in an increase in cytoplasmic free calcium.
Antigen-specific T cell activation results in an increase in cytoplasmic free calcium.
复制标题
DOI：
10.4049/jimmunol.135.4.2256
复制
发表时间：
1985-10
影响因子：
4.4
通讯作者：
D. Shapiro;B. Adams;J. Niederhuber
中科院分区：
文献类型：
--
作者：
D. Shapiro;B. Adams;J. Niederhuber
细胞内游离钙作为信使响应细胞外刺激，包括那些导致细胞增殖。例如，促有丝分裂凝集素已显示在T淋巴细胞增殖期间增加细胞内钙浓度（[Ca+2]i）。为了确定当T细胞被标称抗原激活时是否发生[Ca +2]i的类似变化，通过使用钙敏感性荧光quin-2在来自牛胰岛素特异性、主要组织相容性限制性T杂交瘤的鼠T细胞中测量[Ca+2]i。通过与抗原脉冲的抗原呈递细胞（APC）孵育来活化负载Quin-2的T杂交瘤细胞，并通过测量quin-2荧光来测定[Ca+2]i。T细胞[Ca+2]i在与APC孵育后20 min内迅速升高。T细胞与非脉冲APC的孵育导致[Ca+2]i与静息水平没有显著差异。进一步的证据表明，这种激活是抗原特异性的，在APC和T细胞的水平。将负载quin-2的T细胞与用不适当的抗原（猪胰岛素）脉冲的APC孵育，没有导致[Ca+2]i的增加。此外，用抗T细胞抗原受体的单克隆抗体预处理T细胞可消除[Ca+2]i的增加。最后，抗原诱导的[Ca+2]i升高可以通过用适当但不适当的Ia单克隆抗体预处理APC来阻断。这些结果表明，[Ca+2]i的快速上升是T细胞抗原特异性活化的早期事件，并可能与随后的步骤有关，如淋巴细胞单核因子的分泌。
Free intracellular calcium acts as a messenger in response to extracellular stimuli, including those that result in cellular proliferation. For example, mitogenic lectins have been shown to increase intracellular calcium concentration ([Ca+2]i) during proliferation of T lymphocytes. To determine if similar changes in [Ca+2]i occur when T cells are activated by nominal antigen, [Ca+2]i was measured in murine T cells from a bovine insulin-specific, major histocompatibility-restricted T hybridoma by using the calcium-sensitive fluor quin-2. Quin-2-loaded T hybridoma cells were activated by incubation with antigen-pulsed antigen-presenting cells (APC) and [Ca+2]i determined by measurement of quin-2 fluorescence. T cell [Ca+2]i rose sharply within 20 min after incubation with APC. Incubation of T cells with unpulsed APC resulted in [Ca+2]i not significantly different from resting levels. Further evidence that this activation was antigen specific was demonstrated at the level of both the APC and the T cell. Incubation of quin-2-loaded T cells with APC pulsed with the inappropriate antigen, porcine insulin, did not result in an increase in [Ca+2]i. Additionally, pretreatment of T cells with a monoclonal antibody against the T cell antigen receptor abrogated the [Ca+2]i increase. Finally, the antigen-induced rise in [Ca+2]i could be blocked by pretreatment of APC with appropriate but not inappropriate Ia monoclonal antibodies. These results suggest that a rapid rise in [Ca+2]i is an early event in the antigen-specific activation of the T cell and may be related to later steps, such as the secretion of lymphocyte monokines.