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对移植B6-lpr脾细胞的B6小鼠中移植物抗宿主样疾病机制的分析。

Analysis of the mechanism of graft-versus-host-like disease in B6 mice with transferred B6-lpr spleen cells.

作者信息

Matsunaga T, Kobayashi S, Harada H, Kawaguchi Y, Wang W, Okuyama H

机构信息

Section of Immunopathogenesis, Hokkaido University, Sapporo, Japan.

出版信息

Autoimmunity. 1991;8(4):307-15. doi: 10.3109/08916939109007638.

Abstract

Irradiated C57BL/6(B6) mice, when they were injected with spleen cells of C57BL/6J-lpr/lpr(B6-lpr) mice, developed splenomegaly at 2 weeks post-transfer, but afterward displaced by GVH-like disease. At 2 weeks the enlarged spleen in the chimeric mice, designated as [B6-lpr----B6] chimera, contained about 70% of the total cell population as CD8-positive T cells. Spleen cells from [B6-lpr----B6] chimeras were unresponsive to Con A and LPS stimulation and suppressed the mitogenic response of B6, B6-lpr, and C3H spleen cells to Con A. However, they had no cytotoxic activity towards Con A blasts of B6 and B6-lpr spleen cells. The suppressor activity found in the [B6-lpr----B6] spleen cells was removed by pretreatment of them with anti-Thy-1.2 or anti-CD8(Lyt2.2) plus complement. The present experiment showed that enormous proliferation of CD8-positive suppressor T cells was induced in the [B6-lpr----B6] chimeras. These cells were probably responsible for the GVH-like lymphoid atrophy observed in these [B6-lpr----B6] chimeras.

摘要

用C57BL/6J-lpr/lpr(B6-lpr)小鼠的脾细胞注射经照射的C57BL/6(B6)小鼠后,在转移后2周出现脾肿大,但随后被类似移植物抗宿主病的病症所取代。在2周时,嵌合小鼠(命名为[B6-lpr----B6]嵌合体)肿大的脾脏中,约70%的细胞群体为CD8阳性T细胞。[B6-lpr----B6]嵌合体的脾细胞对刀豆蛋白A(Con A)和脂多糖(LPS)刺激无反应,并抑制B6、B6-lpr和C3H脾细胞对Con A的促有丝分裂反应。然而,它们对B6和B6-lpr脾细胞的Con A母细胞没有细胞毒性活性。用抗Thy-1.2或抗CD8(Lyt2.2)加补体预处理[B6-lpr----B6]脾细胞后,其发现的抑制活性被消除。本实验表明,在[B6-lpr----B6]嵌合体中诱导了CD8阳性抑制性T细胞的大量增殖。这些细胞可能是导致这些[B6-lpr----B6]嵌合体中观察到的类似移植物抗宿主病的淋巴萎缩的原因。

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