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二乙基二硫代氨基甲酸钠(DTC,ImuthiolR)对老年BALB/c小鼠T细胞缺陷反应的影响。

Influences of sodium diethyldithiocarbamate, DTC (imuthiolR) on T cell defective responses of aged BALB/c mice.

作者信息

Bruley-Rosset M, Vergnon I, Renoux G

出版信息

Int J Immunopharmacol. 1986;8(3):287-97. doi: 10.1016/0192-0561(86)90110-4.

Abstract

The effect of chronic imuthiol treatment, 25 mg/kg weekly for 4 months initiated at the age of 12 months, on T-cell functions of aged female BALB/c mice was investigated. Imuthiol restored to normal value the impaired response to Concanavalin A (Con A) and enhanced the proliferative response to phytohemagglutinin (PHA). Impaired cytotoxic T-cell activity (CTL), was restored near to the value of young controls by imuthiol. Serum thymic factor (FTS) levels in serum of treated aged animals outpassed those of untreated young mice. Delayed-type hypersensitivity (DTH) reaction to oxazolone was increased. In contrast, the graft-vs-host (GVH) mortality induced by injecting H-2 histoincompatible cells to irradiated recipients, which GVH was impaired by aging, was not significantly modified by imuthiol. The excessive cytotoxicity for chicken red cells of macrophages (ADCC) from aged mice was reduced, as well as macrophage cytotoxicity for tumor cells. Natural killer cell activity remained unchanged. This finding confirms that imuthiol enhanced effectively T cell-dependent responses but the data on GVH reaction suggest that its effects are under a complex mode of action. Restoration of a normal production of FTS may be one mechanism by which imuthiol acts on the reinduction of the T-cell differentiating pathway in aged mice.

摘要

研究了对12月龄开始每周给予25mg/kg硫普罗宁、持续4个月的慢性硫普罗宁治疗,对老龄雌性BALB/c小鼠T细胞功能的影响。硫普罗宁使对刀豆球蛋白A(Con A)受损的反应恢复至正常水平,并增强了对植物血凝素(PHA)的增殖反应。硫普罗宁使受损的细胞毒性T细胞活性(CTL)恢复至接近年轻对照的值。经治疗的老龄动物血清中的血清胸腺因子(FTS)水平超过未治疗的年轻小鼠。对恶唑酮的迟发型超敏反应(DTH)增强。相反,向经照射的受体注射H-2组织不相容细胞所诱导的移植物抗宿主(GVH)死亡率(衰老会使其受损)未因硫普罗宁而发生显著改变。老龄小鼠巨噬细胞对鸡红细胞的过度细胞毒性(ADCC)降低,对肿瘤细胞的巨噬细胞细胞毒性也降低。自然杀伤细胞活性保持不变。这一发现证实硫普罗宁有效增强了T细胞依赖性反应,但关于GVH反应的数据表明其作用处于复杂的作用模式。FTS正常产生的恢复可能是硫普罗宁作用于老龄小鼠T细胞分化途径再诱导的一种机制。

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