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NZB/W小鼠自身免疫发病机制中抑制性T细胞的缺失。

Loss of suppressor T cells in the pathogenesis of the autoimmunity of NZB/W mice.

作者信息

Krakauer R S, Strober W, Waldmann T A

出版信息

Arthritis Rheum. 1978 Jun;21(5 Suppl):S185-9. doi: 10.1002/art.1780210931.

Abstract

Loss of suppressor T cells was demonstrated in NZB/W mice, an animal model of autoimmunity. As NZB/W mice matured they lost splenic T cells that could be activated by concanavalin A (Con A) to become suppressor cells and lost the ability to produce the regulator of humoral immune responses, soluble immune response suppressor (SIRS). However, NZB/W spleen cells retained the capacity to respond to suppressor signals from Con A pulsed normal spleen cells. Thrice weekly administration of SIRS containing supernatants of Con A pulsed normal spleen cells to young NZB/W mice lead to a striking reduction in the manifestations of autoimmunity.

摘要

在自身免疫动物模型NZB/W小鼠中证实了抑制性T细胞的缺失。随着NZB/W小鼠的成熟,它们失去了可被刀豆蛋白A(Con A)激活而成为抑制性细胞的脾脏T细胞,并失去了产生体液免疫反应调节因子——可溶性免疫反应抑制因子(SIRS)的能力。然而,NZB/W脾细胞保留了对来自Con A刺激的正常脾细胞抑制信号作出反应的能力。每周三次给年轻的NZB/W小鼠注射含有Con A刺激的正常脾细胞上清液的SIRS,可显著降低自身免疫的表现。

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