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来自干扰素-γ基因敲除小鼠的CD45RB高表达CD4⁺ T细胞不会诱发消瘦症。

CD45RBhigh CD4+ T cells from IFN-gamma knockout mice do not induce wasting disease.

作者信息

Ito H, Fathman C G

机构信息

Department of Medicine, Stanford University School of Medicine, Stanford, California 94305, USA.

出版信息

J Autoimmun. 1997 Oct;10(5):455-9. doi: 10.1016/s0896-8411(97)90152-9.

Abstract

Transfer of CD45RBhigh CD4+ T cells from normal mice to congenic SCID mice induces wasting disease, a murine model of inflammatory bowel disease. In this model, colonic inflammation is considered to be caused by a disregulated Th1 response, and Th1 cytokines, especially IFN-gamma, have been suggested to play an important role in the pathogenesis of wasting disease. In order to elucidate the potential role of IFN-gamma in the pathogenesis of wasting disease, we transferred CD45RBhigh CD4+ T cells from IFN-gamma knockout (GKO) mice to congenic SCID mice. The recipient mice were absolutely free of symptoms and clinical signs of disease and showed body-weight gain similar to that seen in normal mice. These data demonstrate the essential and non-redundant role of IFN-gamma in the pathogenesis of wasting disease.

摘要

将正常小鼠的CD45RB高表达CD4 + T细胞转移至同基因SCID小鼠中可诱发消瘦病,这是一种炎症性肠病的小鼠模型。在该模型中,结肠炎症被认为是由失调的Th1反应引起的,并且Th1细胞因子,尤其是干扰素-γ,被认为在消瘦病的发病机制中起重要作用。为了阐明干扰素-γ在消瘦病发病机制中的潜在作用,我们将来自干扰素-γ基因敲除(GKO)小鼠的CD45RB高表达CD4 + T细胞转移至同基因SCID小鼠中。受体小鼠完全没有疾病的症状和体征,并且体重增加情况与正常小鼠相似。这些数据证明了干扰素-γ在消瘦病发病机制中的关键和不可替代的作用。

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