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早期同种异体反应期间脑皮质细胞或淋巴细胞的细胞表面酶。

Cell surface enzymes of brain cortex cells or lymphocytes during early allogeneic reaction.

作者信息

Kovárů H, Kovárů F, Hasková V

机构信息

First Medical Faculty, Charles University, Prague, Czech Republic.

出版信息

Physiol Res. 1997;46(2):137-44.

PMID:9727505
Abstract

The aim was to study the role of major histocompatibility complex (MHC), in mice named H-2, during early allogeneic reactions (AR) of brain cortex cells or lymphocytes. We used neuronal and glial enriched perikarya, spleen and thymus lymphocytes or their subpopulations. Rat AR was also assayed between C-6 astrocytoma cells and spleen lymphocytes. We demonstrated that: 1) H-2 dependent stimulation of Na+,K+-ATPase and ouabain-sensitive K+-dependent p-nitrophenylphosphatase (K+-pNPPase) activities represented specific response in both AR of unseparated brain cells or lymphocytes. On the other hand, non-specific AR-induced stimulation of Ca2+-ATPase activity was observed. 2) Allogeneic enriched glial fractions reacted similarly by the same enzyme activation in contrast to no change in AR between enriched neuronal fractions. Allorecognition ability of glial cells was confirmed by AR between C-6 astrocytoma cells and lymphocytes. 3) Mature thymus lymphocytes exerted alloreactivity by specific activation of Na+,K+-ATPase or K+-pNPPase, in contrast to no change in AR between immature lymphocyte subpopulations. 4) MHC Class II monoclonal antibody inhibited Na+,K+-ATPase and K+-pNPPase activities in brain cells as well as in thymus and spleen lymphocytes in a dose-dependent manner. Results support former studies about alloantigen-induced uncoupling in brain oxidative cortex metabolism (Kovárů Med. Biol. 58: 273, 1980) via Na+,K+-ATPase and K+-pNPPase inhibition by mechanism which can mimic MHC restriction.

摘要

目的是研究主要组织相容性复合体(MHC),即小鼠体内的H-2,在脑皮质细胞或淋巴细胞早期同种异体反应(AR)中的作用。我们使用了富含神经元和神经胶质的核周体、脾和胸腺淋巴细胞或它们的亚群。还检测了C-6星形细胞瘤细胞与脾淋巴细胞之间的大鼠AR。我们证明:1)H-2依赖性刺激Na +,K + -ATP酶和哇巴因敏感的K +依赖性对硝基苯磷酸酶(K + -pNPPase)活性代表了未分离的脑细胞或淋巴细胞的AR中的特异性反应。另一方面,观察到非特异性AR诱导的Ca2 + -ATP酶活性刺激。2)同种异体富集的神经胶质部分通过相同的酶激活表现出相似的反应,而富集的神经元部分之间的AR没有变化。C-6星形细胞瘤细胞与淋巴细胞之间的AR证实了神经胶质细胞的同种异体识别能力。3)成熟的胸腺淋巴细胞通过Na +,K + -ATP酶或K + -pNPPase的特异性激活发挥同种异体反应性,而未成熟淋巴细胞亚群之间的AR没有变化。4)MHC II类单克隆抗体以剂量依赖性方式抑制脑细胞以及胸腺和脾淋巴细胞中的Na +,K + -ATP酶和K + -pNPPase活性。结果支持了以前关于同种异体抗原通过Na +,K + -ATP酶和K + -pNPPase抑制诱导脑氧化皮质代谢解偶联的研究(Kovárů医学与生物学杂志58:273,1980),其机制可模拟MHC限制。

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