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培养的小鼠细胞毒性T淋巴细胞中缺乏腺苷脱氨酶活性。

Lack of adenosine deaminase activity in cultured murine cytotoxic T lymphocytes.

作者信息

Minkowski M D, Castellazzi M, Buttin G

出版信息

J Immunol. 1984 Jul;133(1):52-8.

PMID:6609994
Abstract

The level of adenosine deaminase (ADA) activity was investigated in various populations of IL 2-dependent, cultured cytotoxic T lymphocytes (CTL), from bulk cultures as well as from CTL lines (CTL-A and CTL-B types). The study of C57BL/6 derived, cytotoxic bulk cultures yielded the following mean values of ADA activity: 12,500 U/mg in the cortical, immature region of the thymus, 1500 U/mg in the immunocompetent, cortisone-resistant medullary thymocytes, and 2000 U/mg in the T cell population from the spleen. These results are in agreement with previous studies on separated T lymphocyte populations of known origin and further indicate that a fall in ADA activity accompanies T cell maturation. ADA activity was measured in C57BL/6-derived CTL-A lines obtained from the thymic and splenic bulk cultures. All lines were characterized by a very low level of ADA activity, compared with the T cell bulk cultures freshly initiated from the thymic medulla or from the spleen, and to a variety of T tumor lines established in long term culture. Some showed undetectable ADA activity (less than or equal to 20 units/mg), whereas others maintained significant activity (50 to 500 U/mg). No correlation was found between the residual ADA activity level and the killing activity, at the time of the enzyme assay. Identical properties were observed for CTL-B cloned lines of various genetic backgrounds. These results suggest that the level of ADA activity of the CTL in the mouse is lower than the average value of mature T cells of the thymic medulla, and might constitute a differentiation marker specific to the CTL population. A possibility remains that low ADA activity levels in these CTL lines may be the consequence of an extinction of the ADA gene during in vitro growth, as it is observed for the cytotoxic activity itself. In either case, a low ADA activity level is a remarkable property of IL 2-dependent CTL clones, when compared to various established T tumor lines, which exhibit high and stable ADA levels during long term in vitro growth (5000 to 15,000 U/mg).

摘要

在来自大量培养物以及CTL系(CTL - A和CTL - B型)的各种白细胞介素2依赖性培养细胞毒性T淋巴细胞(CTL)群体中,研究了腺苷脱氨酶(ADA)活性水平。对源自C57BL / 6的细胞毒性大量培养物的研究得出了以下ADA活性的平均值:胸腺皮质未成熟区域为12,500 U/mg,具有免疫活性、耐可的松的髓质胸腺细胞为1500 U/mg,脾脏T细胞群体为2000 U/mg。这些结果与先前对已知来源的分离T淋巴细胞群体的研究一致,并进一步表明ADA活性的下降伴随着T细胞成熟。在从胸腺和脾脏大量培养物中获得的源自C57BL / 6的CTL - A系中测量了ADA活性。与从胸腺髓质或脾脏新起始的T细胞大量培养物以及长期培养中建立的各种T肿瘤系相比,所有系的ADA活性水平都非常低。一些显示无法检测到的ADA活性(小于或等于20单位/mg),而其他系则保持显著活性(50至500 U/mg)。在酶测定时,未发现残余ADA活性水平与杀伤活性之间存在相关性。对于各种遗传背景的CTL - B克隆系,观察到了相同的特性。这些结果表明,小鼠中CTL的ADA活性水平低于胸腺髓质成熟T细胞的平均值,并且可能构成CTL群体特有的分化标志物。仍然存在一种可能性,即这些CTL系中低ADA活性水平可能是体外生长过程中ADA基因灭绝的结果,就像细胞毒性活性本身一样。在任何一种情况下,与各种已建立的T肿瘤系相比,低ADA活性水平都是白细胞介素2依赖性CTL克隆的显著特性,这些T肿瘤系在长期体外生长过程中表现出高且稳定的ADA水平(5000至15,000 U/mg)。

相似文献

1
Lack of adenosine deaminase activity in cultured murine cytotoxic T lymphocytes.培养的小鼠细胞毒性T淋巴细胞中缺乏腺苷脱氨酶活性。
J Immunol. 1984 Jul;133(1):52-8.
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Azacytidine-induced reactivation of adenosine deaminase in a murine cytotoxic T cell line.
Eur J Immunol. 1986 Sep;16(9):1081-6. doi: 10.1002/eji.1830160909.
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Different functional subsets of cultured murine T cells express characteristic levels of adenosine deaminase activity.培养的小鼠T细胞的不同功能亚群表达特征水平的腺苷脱氨酶活性。
Cell Immunol. 1985 Oct 15;95(2):380-91. doi: 10.1016/0008-8749(85)90325-9.
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Reversibility of lymphokine-induced NK-like activity in virus-specific cytotoxic T-lymphocyte clones.病毒特异性细胞毒性T淋巴细胞克隆中淋巴因子诱导的NK样活性的可逆性
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Induction of suppressor T cells by interleukin 2.白细胞介素2诱导抑制性T细胞
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[Age-dependence of adenosine deaminase activity in mouse lymphocytes from the spleen and thymus].[小鼠脾脏和胸腺淋巴细胞中腺苷脱氨酶活性的年龄依赖性]
Allerg Immunol (Leipz). 1984;30(4):207-11.
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Isolation and characterization of novel suppressor T cell clones from murine fetal thymus.从小鼠胎儿胸腺中分离并鉴定新型抑制性T细胞克隆。
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A helper factor needed for the generation of mouse cytolytic T lymphocytes is made by tumor cell lines, cloned T cells, and spleen cells exposed to a variety of stimuli.一种生成小鼠细胞毒性T淋巴细胞所需的辅助因子由肿瘤细胞系、克隆T细胞以及受到多种刺激的脾细胞产生。
J Immunol. 1984 Jul;133(1):502-8.

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