12-O-Tetradecanoylphorbol-13-acetate (TPA) directly inhibits spontaneous immunoglobulin secretion by in vivo antigen-induced human lymphoblastoid B cells.
12-O-Tetradecanoylphorbol-13-acetate (TPA) directly inhibits spontaneous immunoglobulin secretion by in vivo antigen-induced human lymphoblastoid B cells.
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12-O-Tetradecanoylphorbol-13-acetate (TPA) 直接抑制体内抗原诱导的人淋巴母细胞 B 细胞的自发免疫球蛋白分泌。
DOI：
10.1007/bf00915295
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发表时间：
1984
影响因子：
9.1
通讯作者：
Stevens,RH
中科院分区：
文献类型：
--
作者：
Brieva,JA;Louie,JS;Stevens,RH
破伤风类毒素（泰特）加强免疫诱导类淋巴母细胞（LB）B细胞在循环中短暂出现，在3天的体外培养期间，LB B细胞自发产生抗破伤风类毒素IgG抗体（IgG-泰特）。在这项研究中，我们已经检查了TPA对LB细胞分泌抗体的能力的影响，并发现低至10 ng/ml的TPA引起对诱导的LB细胞的IgG-Tet产生的显著抑制。这种抑制作用只有在培养早期加入TPA时才能观察到，并且可以通过用TPA预处理B细胞短至1小时来实现。TPA抑制不是由污染物T细胞介导的，因为向LB细胞培养物中添加增加数量的T细胞成比例地逆转了TPA抑制。TPA抑制作用。同样地，抗体合成的抑制不是由于单核细胞依赖性机制，因为（1）粘附细胞的大量消耗没有逆转抗体合成的抑制，（2）向单核细胞消耗的B细胞中加入富含单核细胞的群体没有增强，但事实上部分逆转了TPA引起的抑制，和（3）将TPA预处理的单核细胞群加入到单核细胞耗尽的B细胞级分中不会抑制LB细胞随后的IgG-Tet产生。
Tetanus toxoid (Tet) booster immunization induces the transient appearance in the circulation of lymphoblastoid (LB) B cells which spontaneously produce anti-tetanus toxoid IgG antibody (IgG-Tet) during a 3-dayin vitroculture. In this study we have examined the effects of TPA on the ability of LB cells to secrete antibody and have found that as little as 10 ng/ml of TPA provoked a marked inhibition of the induced LB cells' IgG-Tet production. This inhibitory effect was observed only when TPA was added early in the culture and could be achieved by pretreating the B cells with TPA for as little as 1 hr. Only marginal inhibition of IgG-Tet production was observed if the addition of TPA was delayed 14–24 hr. The TPA inhibition was not mediated by contaminant T cells as the addition of increasing numbers of T cells to LB cell cultures proportionally reversed the TPA inhibitory effect. Likewise, the inhibition of antibody synthesis was not due to a monocyte-dependent mechanism since (1) substantial depletion of adherent cells did not reverse the inhibition of antibody synthesis, (2) the addition of a monocyte-enriched population to monocyte-depleted B cells did not enhance, but in fact partially reversed, the inhibition caused by TPA, and (3) the addition of monocyte populations pretreated with TPA to monocyte-depleted B-cell fractions did not inhibit subsequent IgG-Tet production by the LB cells.