Activation of resting T lymphocytes by anti-CD3 (T3) antibodies in the absence of monocytes.
Activation of resting T lymphocytes by anti-CD3 (T3) antibodies in the absence of monocytes.
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DOI：
10.4049/jimmunol.135.3.1719
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发表时间：
1985-09
影响因子：
4.4
通讯作者：
C. Tsoukas;B. Landgraf;J. Bentin;M. Valentine;M. Lotz;J. Vaughan;D. Carson
中科院分区：
文献类型：
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作者：
C. Tsoukas;B. Landgraf;J. Bentin;M. Valentine;M. Lotz;J. Vaughan;D. Carson
人T淋巴细胞上的抗原受体分子在细胞表面上与CD 3（T3）分子复合物非共价结合。用抗CD 3单克隆抗体干扰该复合物可诱导T细胞活化。以前的研究表明，这一过程需要单核细胞的参与。在本报告中，我们证明，纯化的，休息（G 0期）T细胞与单克隆抗CD 3抗体孵育增殖响应纯化的白细胞介素2（IL 2），在淋巴因子剂量依赖性的方式。单独使用抗CD 3抗体或IL-2并不引起细胞分裂。该效应对于抗CD 3抗体是特异性的，因为与其他表面分子（OKT 4、OKT 8、L368）反应的单克隆抗体是无活性的。此外，当抗CD 3抗体Leu-4（IgG 1）与单核细胞不能处理IgG 1亚类抗体的个体（Leu-4无应答者）的细胞孵育时，观察到相同的现象。此外，抗CD 3抗体OKT 3的F（ab '）2和Fab片段也能够使T细胞接受IL 2生长信号。这些数据表明，单核细胞和CD 3受体交联都不是静止T细胞活化所绝对需要的，只要外源性提供IL 2。用抗CD 3抗体处理的T淋巴细胞对纯化的丝裂原诱导的和重组的IL 2都有反应。IL-2受体抗体（anti-Tac）可抑制细胞增殖。因此，抗CD 3抗体介导的触发最可能的机制是诱导IL 2受体。
The antigen receptor molecules on human T lymphocytes are noncovalently associated on the cell surface with the CD3 (T3) molecular complex. Perturbation of this complex with anti-CD3 monoclonal antibodies induces T cell activation. Previous studies have demonstrated that this process requires the participation of monocytes. In the present report, we demonstrate that purified, resting (G0 phase) T cells incubated with monoclonal anti-CD3 antibodies proliferate in response to purified interleukin 2 (IL 2), in a lymphokine dose-dependent fashion. Anti-CD3 antibody or IL 2 alone did not trigger cell division. The effect was specific for anti-CD3 antibodies because monoclonal antibodies reactive with other surface molecules (OKT4, OKT8, L368) were inactive. Furthermore, the same phenomenon was observed when anti-CD3 antibody Leu-4 (IgG1) was incubated with cells of individuals whose monocytes cannot process antibodies of the IgG1 subclass (Leu-4 nonresponders). In addition, both F(ab')2 and Fab fragments of anti-CD3 antibody OKT3 were also capable of rendering T cells receptive to the IL 2 growth signal. These data indicate that neither monocytes nor CD3 receptor cross-linking are required absolutely for resting T cell activation, provided that IL 2 is supplied exogenously. T lymphocytes treated with anti-CD3 antibodies proliferated in response to both purified mitogen-induced and recombinant IL 2. Antibodies to the IL 2 receptor (anti-Tac) inhibited the proliferation. Thus, the most likely mechanism for anti-CD3 antibody-mediated triggering is induction of IL 2 receptors.