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一种合成逆转录病毒肽对小鼠细胞毒性T淋巴细胞活性的抑制作用以及白细胞介素对该活性的消除作用。

Inhibition of murine cytotoxic T lymphocyte activity by a synthetic retroviral peptide and abrogation of this activity by IL.

作者信息

Ogasawara M, Haraguchi S, Cianciolo G J, Mitani M, Good R A, Day N K

机构信息

All Children's Hospital, University of South Florida College of Medicine, St. Petersburg 33701.

出版信息

J Immunol. 1990 Jul 15;145(2):456-62.

PMID:2195116
Abstract

A synthetic 17 amino acid peptide (CKS-17) homologous to a highly conserved region of human and animal retroviral transmembrane proteins was investigated for its influence on the generation of murine alloantigen-specific CTL activity in vitro. CKS-17 coupled to a carrier protein, BSA or human serum albumin, inhibited the generation of anti-allo CTL in a dose-dependent manner. Controls consisting of BSA and human serum albumin, which had undergone the coupling procedure or neurotensin, an unrelated peptide, coupled to BSA in an identical manner as CKS-17 showed no such inhibitory action. The suppression was not restricted to the Ag specificity of the CTL activity. CKS-17 exerted inhibitory effects on the early afferent phase of CTL induction. Kinetic studies showed that the suppressive activity occurred when CKS-17 was introduced to the immunologically stimulating culture concomitant with or up to 48 h after initiation of culture. Analysis of the frequency of CTL precursor cells using limiting-dilution assays revealed that CKS-17 did act to reduce the number of precursor cells. Abrogation of the inhibition of CTL activity was observed when IL-2 was introduced to the culture together with the stimulator cells. Other lymphokines, such as IL-4, exerted a similar influence to counteract this suppression.

摘要

研究了一种与人类和动物逆转录病毒跨膜蛋白高度保守区域同源的合成17氨基酸肽(CKS-17)对体外小鼠同种异体抗原特异性CTL活性产生的影响。与载体蛋白牛血清白蛋白(BSA)或人血清白蛋白偶联的CKS-17以剂量依赖性方式抑制抗同种异体CTL的产生。由经过偶联程序的BSA和人血清白蛋白或与CKS-17以相同方式偶联至BSA的无关肽神经降压素组成的对照未显示出这种抑制作用。这种抑制不限于CTL活性的抗原特异性。CKS-17对CTL诱导的早期传入阶段发挥抑制作用。动力学研究表明,当在培养开始时或培养开始后长达48小时将CKS-17引入免疫刺激培养物中时,会出现抑制活性。使用有限稀释测定法分析CTL前体细胞的频率表明,CKS-17确实起到了减少前体细胞数量的作用。当将IL-2与刺激细胞一起引入培养物中时,观察到CTL活性抑制作用的消除。其他细胞因子,如IL-4,也发挥了类似的作用来抵消这种抑制。

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