Grenier-Brossette N, Bourget I, Breittmayer J P, Ferrua B, Fehlmann M, Cousin J L
INSERM U210, Faculté de Médecine (Pasteur) Nice, France.
Immunopharmacology. 1991 Mar-Apr;21(2):109-19. doi: 10.1016/0162-3109(91)90014-p.
Pertussis toxin (PT) has previously been shown to affect a wide variety of immune responses and to cause lymphocyte proliferation. We have investigated the biochemical basis for the mitogenic activity of PT by using human peripheral blood lymphocytes. PT was found to induce a rapid rise in cytosolic free calcium concentration and an alkalinization of the cytosol through the Na+/H+ antiporter. The toxin was also found to induce expression of IL-2-receptor on CD3+ cells and to stimulate IL-2 production. PT induced proliferation of both CD4+ and CD8+ T cells in the presence (but not in the absence) of accessory cells. PT also stimulated IL-1 production by monocytes but neither IL-1, IL-6 alone nor a combination of the two lymphokines could replace accessory cells suggesting that cell:cell contact is required. Low doses of PT induced ADP-ribosylation of G proteins but this treatment did not affect significantly PHA-induced [Ca2+]i increase and IL-2-induced DNA synthesis suggesting that the substrates of the ADP-ribosyltransferase activity of PT are not involved in the signalling pathways leading to DNA replication.
百日咳毒素（PT）先前已被证明会影响多种免疫反应并导致淋巴细胞增殖。我们通过使用人外周血淋巴细胞研究了PT促有丝分裂活性的生化基础。发现PT可通过Na+/H+反向转运体诱导胞质游离钙浓度迅速升高和胞质碱化。还发现该毒素可诱导CD3+细胞上IL-2受体的表达并刺激IL-2的产生。在有辅助细胞存在（但无辅助细胞时则无此作用）的情况下，PT可诱导CD4+和CD8+ T细胞增殖。PT还可刺激单核细胞产生IL-1，但单独的IL-1、IL-6或这两种淋巴因子的组合均不能替代辅助细胞，这表明需要细胞间接触。低剂量的PT可诱导G蛋白的ADP-核糖基化，但这种处理对PHA诱导的[Ca2+]i增加和IL-2诱导的DNA合成没有显著影响，这表明PT的ADP-核糖基转移酶活性的底物不参与导致DNA复制的信号通路。
