Patrignani P, Valitutti S, Aiello F, Musiani P
Department of Pharmacology, Catholic University School of Medicine, Rome, Italy.
Biochem Biophys Res Commun. 1987 Oct 29;148(2):802-10. doi: 10.1016/0006-291x(87)90947-8.
The addition of L-652,731 and L-653,150, two synthetic PAF-specific receptor antagonists, to 72 hour cultures of phytohemagglutinin (PHA)-stimulated human peripheral blood mononuclear leukocytes (PBML) caused a dose-dependent inhibition of (3H)-thymidine incorporation into T-cells (IC50: 25 microM and 3.2 microM, respectively). This inhibition was not reversed by exogenous interleukin (IL)-1 and IL-2. PAF receptor antagonists did not affect the expression of IL-2 receptors (TAC-antigen) on T-cells. Exogenous PAF which by itself had no significant effect on PHA-stimulated PBML proliferation, only partially reversed the inhibition of proliferation caused by PAF receptor antagonists. These results may suggest the involvement of endogenously produced PAF in the regulation of immune reactions.
向植物血凝素（PHA）刺激的人外周血单个核白细胞（PBML）进行72小时培养物中添加两种合成的PAF特异性受体拮抗剂L-652,731和L-653,150，会导致（3H）-胸苷掺入T细胞受到剂量依赖性抑制（IC50分别为25微摩尔和3.2微摩尔）。这种抑制作用不能被外源性白细胞介素（IL）-1和IL-2逆转。PAF受体拮抗剂不影响T细胞上IL-2受体（TAC抗原）的表达。外源性PAF本身对PHA刺激的PBML增殖没有显著影响，只能部分逆转PAF受体拮抗剂引起的增殖抑制。这些结果可能提示内源性产生的PAF参与免疫反应的调节。
