Matsuura T, Negita M, Ikegami M, Imanishi M, Nishioka T, Ishii T, Uemura T, Kunikata S, Kanda H, Akiyama T
Department of Urology, Kinki University School of Medicine.
Hinyokika Kiyo. 1991 Oct;37(10):1141-5.
We applied cloned human T lymphocytes established in our laboratory to evaluate the mode of action of Cyclosporine (CsA) and FK506. Phenotypic and functional analysis led us to conclude that HTL403 was a helper T cell clone and HTL805 a cytotoxic one. Susceptibility of HTL-403 to the immunosuppressants demonstrated that alloantigen-driven proliferative response can recover to the rIL2-driven level by the addition of rIL2 at higher concentration of the agents. Although full recovery was not observed in FK506, this finding indicated that FK506 as well as CsA inhibit IL2 secretion from HTL403. FK506 showed remarkable suppressive effect on the proliferative response of HTL-805 even at a considerably low concentration, while CsA suppressed such a response dose-dependently. We concluded that FK506 can be used to reverse ongoing acute rejection as well as to prevent acute rejection.
我们应用在本实验室建立的克隆化人T淋巴细胞来评估环孢素（CsA）和FK506的作用方式。表型和功能分析使我们得出结论，HTL403是辅助性T细胞克隆，HTL805是细胞毒性T细胞克隆。HTL - 403对免疫抑制剂的敏感性表明，在较高浓度的药物作用下，通过添加rIL2，同种异体抗原驱动的增殖反应可恢复到rIL2驱动的水平。虽然在FK506作用下未观察到完全恢复，但这一发现表明FK506和CsA一样抑制HTL403分泌IL2。即使在相当低的浓度下，FK506对HTL - 805的增殖反应也显示出显著的抑制作用，而CsA则呈剂量依赖性地抑制这种反应。我们得出结论，FK506可用于逆转正在进行的急性排斥反应以及预防急性排斥反应。
