The regulation of the expression of gp39, the CD40 ligand, on normal and cloned CD4+ T cells.
The regulation of the expression of gp39, the CD40 ligand, on normal and cloned CD4+ T cells.
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DOI：
10.4049/jimmunol.151.5.2497
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发表时间：
1993-09
影响因子：
4.4
通讯作者：
M. Roy;T. Waldschmidt;A. Aruffo;J. Ledbetter;R. Noelle
中科院分区：
文献类型：
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作者：
M. Roy;T. Waldschmidt;A. Aruffo;J. Ledbetter;R. Noelle
研究表明，CD40的配体gp39可诱导B细胞周期进入，并参与启动体液免疫反应。在正常、活化的CD4+T细胞、活化的淋巴结细胞、活化的Th1克隆和活化的Th2克隆上已经观察到gp39的表达。抗CD3激活的CD8+T细胞不表达gp39；而经PMA/离子霉素激活的CD8+T细胞表达gp39。抗CD3诱导的gp39在T细胞克隆和脾CD4+T细胞上表达的动力学研究表明，gp39在激活后4h即可检测到，在激活后6~8h达到最高水平，在24~48h恢复到接近静止水平，淋巴因子对激活的T细胞上gp39的表达有调节作用。干扰素-γ抑制活化的Th1、Th2和CD4+T细胞上gp39的表达；而转化生长因子-β仅抑制所研究的Th2克隆上的gp39表达。所有其他淋巴因子测试都没有实质性的效果。观察到激活的幼稚T细胞和记忆T细胞上gp39表达的差异，以及对这些亚群上最佳gp39表达的要求的差异。Gp39的表达与效应器功能相关，但表达gp39的抗CD3激活的脾CD4+细胞不具有效应器功能。对gp39分子相对数量的比较表明，激活的Th1克隆表达的gp39分子/细胞数量至少是激活的脾CD4+细胞的20倍。这可能表明活化T细胞上gp39的密度在决定效应器功能中起着重要作用。
Studies have established that gp39, the ligand for CD40, induces B cell cycle entry and is involved in the initiation of the humoral immune response. Expression of gp39 has been observed on normal, activated CD4+ T cells, activated lymph node cells; an activated Th1 clone, and an activated Th2 clone. Anti-CD3-activated CD8+ T cells did not express gp39; however, CD8+ T cells activated with PMA/ionomycin expressed gp39. The kinetics of anti-CD3-induced gp39 expression on a T cell clone and on splenic CD4+ T cells showed that gp39 was detectable at 4 h after activation, reaching maximal levels between 6 to 8 h postactivation and returning to near resting levels between 24 to 48 h. Lymphokines modulated the expression of gp39 on activated T cells. Expression of gp39 was inhibited by IFN-gamma on activated Th1, Th2, and CD4+ T cells; whereas TGF-beta inhibited gp39 expression only on the Th2 clone studied. All other lymphokines tested were without substantial effect. Differences in the expression of gp39 on activated naive and memory T cells were observed, as well as differences in requirements for optimal gp39 expression on these subsets. There are correlations between gp39 expression and effector function; however, anti-CD3-activated splenic CD4+ cells that express gp39 did not exhibit effector function. A comparison of the relative numbers of molecules of gp39 shows that activated Th1 clones express at least 20-fold the number of gp39 molecules/cell compared with activated splenic CD4+ cells. This may imply that density of gp39 on the activated T cells plays an important role in determining effector function.