脾细胞在CTL克隆增殖中的作用

本文证明二次MLC上清或重组IL2均不足以维持细胞毒 T细胞(CTL)克隆的正常增殖,而同种异体、同种第三者、甚至同基因的脾细胞均可增强rIL2诱导的CTL克隆增殖应答,亦可增强 CTL由 CD3∈链抗体(145-2C11)刺激的 IL-2非依赖性增殖。脾细胞的这种辅佐效应似与可溶性因子或脾粘附细胞无关。用 rIL2 预处理的脾细胞可诱导 CTL克隆的显著增殖,这种增殖可被抗IL2 受体抗体所抑制,提示脾细胞可能将其“膜结合”rIL2递给CTL而更有效地诱导增殖反应。FD18.5(抗 LFA-1),KH1.4(抗 Ly-6)及 HK2.1(抗 Thy-1)可显著抑制脾细胞对 145-2C11 激活 CTL增殖的辅佐效应,提示脾细胞对 CTL克隆 IL2非依赖性增殖的辅佐效应与一些细胞表面分子有关。

ROLE OF SPLEEN CELLS IN THE PROLIFERATION OF CTL CIONES

Our works confirmed that the supernatant from a secondary MLC or recombinant IL2 (rIL2) was not sufficient for cloned CTL to proliferate. However, syngeneic, irrelevant as well as allogenic splenocytes were able to enhance both rIL2-driven and 145-2C11 (an antibody reactive with s chain of CD3) induced proliferation in the cloned CTL tested. Soluble factors and adherent population of splenocytes seemed not to contribute to these phenomena. Spleen cells pretreated with rIL2 were found to significantly induce the proliferation. This effect was completely inhibited by the anti-IL2 receptor antibodies, strongly suggesting that the "membrane-bound" rIL2 on the surface of splenocytes was presented to cloned CTL as a potent stimulant. On the other hand, antibodies like FD18.5 (to LFA-1), HZ 1.4 (to Ly-6) and HK2.1 (to Thy-1) markedly inhibited the enhancement of the 145-2011 induced proliferation, suggesting that some molecules on the cell surface were responsible for the accessory effects of splenocytes on the IL-2-independent proliferation of CTLs.