Karagouni E E, Kourounakis L
Department of Genetics, Development and Molecular Biology, School of Biology, Faculty of Sciences, Aristotelian University, Thessaloniki, Greece.
Arzneimittelforschung. 1991 Jun;41(6):647-51.
The novel agent gamma-(2-aminoethylamino-2-butyrothienone (gamma-ABT) has been found to suppress adjuvant induced disease (AID). To explore the mechanism of action of gamma-ABT in AID, the effects of gamma-ABT on suppressor cells, found in AID, and on interleukin production were evaluated. gamma-ABT did not affect the concavalin A (Con A) responses of AID splenocytes when the suppressor plastic-glass and glass-only-adherent cells were removed. gamma-ABT affected the Con A responses of glass-adherent cells indicating that this agent is selectively affecting the glass-adherent suppressor cells. Interleukins 1 and 2 production is augmented by gamma-ABT in normal and AID rats. Since IL-1 abrogated the suppressive effect of glass-adherent suppressor cells, it is suggested that the inhibition of IL-1 mediated events of suppressor cells may be one of the mechanisms of action of gamma ABT in AID. The relevance of the present results to a latent virus etiology of AID is discussed.
新型药物γ-(2-氨乙基氨基)-2-丁基噻吩酮(γ-ABT)已被发现可抑制佐剂诱导的疾病(AID)。为探究γ-ABT在AID中的作用机制,评估了γ-ABT对AID中发现的抑制细胞以及白细胞介素产生的影响。当去除抑制性塑料玻璃贴壁细胞和仅玻璃贴壁细胞时,γ-ABT不影响AID脾细胞对刀豆球蛋白A(Con A)的反应。γ-ABT影响玻璃贴壁细胞对Con A的反应,表明该药物选择性地影响玻璃贴壁抑制细胞。在正常大鼠和AID大鼠中,γ-ABT可增强白细胞介素1和2的产生。由于白细胞介素1消除了玻璃贴壁抑制细胞的抑制作用,因此提示抑制白细胞介素1介导的抑制细胞事件可能是γ-ABT在AID中的作用机制之一。讨论了当前结果与AID潜在病毒病因的相关性。