Virgin and memory T cells have different requirements for activation via the CD2 molecule.

Virgin and memory T cells have different requirements for activation via the CD2 molecule.
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原始 T 细胞和记忆 T 细胞对于通过 CD2 分子激活有不同的要求。

DOI:
10.1093/intimm/1.1.29
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发表时间:
1989
影响因子:
4.4
通讯作者:
Cooper,MD
Cooper,MD
中科院分区:
医学3区
文献类型:
--
作者:
Byrne,JA;Butler,JL;Reinherz,EL;Cooper,MD

文献摘要

被引文献

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T细胞可通过其表达白细胞共同抗原的不同同种型而分为未致敏原始(T°)和致敏记忆(T ')亚群。我们将CD 4 +T细胞分离为T°和T'亚群,并检查了它们通过CD 2受体分子响应激活信号的能力。在用抗-CD 2抗体的促有丝分裂组合刺激时,T'群体被诱导表达IL-2受体,增加4F 2抗原的水平并增殖,而T°群体的应答仅通过4F 2抗原的最小增加来反映。将IL-2或单核细胞添加到用抗CD 2抗体刺激的T°细胞中不会增强它们的IL-2受体表达或增殖。然而,用抗CD 2抗体、单核细胞和IL-2刺激的T°细胞以高水平的IL-2受体表达和增殖应答。T°亚群在与抗CD 2抗体和佛波醇肉豆蔻酸酯乙酸酯一起培养时也可被诱导应答。结果表明,为了通过CD 2分子对刺激做出反应,原始T辅助细胞需要额外的信号,这些信号可以由单核细胞和IL-2共同提供。相反,记忆性T辅助细胞可以单独通过CD 2信号转导激活。
T cells can be divided into unprimed virgin (T°) and primed memory (T') subpopulations by their expression of different isoforms of the leukocyte common antigen. We have separated the CD4+T cells into T° and T' subpopulations and examined their capacity to respond to activation signals via the CD2 receptor molecule. On stimulation with a mitogenic combination of anti-CD2 antibodies, the T' population was inducd to express IL-2 receptor, increased levels of the 4F2 antigen and to proliferate, whereas the response of the T° populations was reflected solely by a minimal increase in the 4F2 antigen. The addition of IL-2 or monocytes to T° cells stimulated with anti-CD2 antibodies did not enhance their expression of the IL-2 receptor or proliferation. However, T° cells stimulated with the tried of anti-CD2 antibodies, monocytes, and IL-2 responded with high levels of IL-2 receptor expression and proliferation. The T° subpopulation could also be induced to respond when cultured with anti-CD2 antibodies and phorbol myristate acetate. The results suggest that in order to respond to stimulation via the CD2 molecule, virgin T helper cells require additional signals that can be jointly provided by monocytes and IL-2. In contrast, memory T helper cells can be activated via CD2 signal transduction alone.