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干扰素α/β在小鼠肠道病理诱导中的作用。

The role of interferon alpha/beta in the induction of intestinal pathology in mice.

作者信息

Garside P, Felstein M V, Green E A, Mowat A M

机构信息

Department of Immunology, University of Glasgow, Western Infirmary.

出版信息

Immunology. 1991 Oct;74(2):279-83.

Abstract

We have investigated the role of interferon-alpha/beta (IFN-alpha/beta) and IFN-dependent effector cells in causing enteropathy in mice. The IFN-inducer polyinosinic:polycytydylic acid (poly I:C) augmented the natural killer (NK) cell activation normally seen in neonatal (CBA x BALB/c)F1 mice with graft-versus-host reaction (GVHR) and exacerbated the systemic and intestinal consequences of GVHR. Poly I:C itself produced a similar pattern of intestinal pathology when administered to normal mice. The effects of poly I:C on NK cell activity and intestinal architecture in normal mice could be reproduced by a single injection of purified IFN-alpha/beta and the intestinal lesions caused by IFN-alpha/beta were prevented by in vivo depletion of NK cells with anti-asialo GM1. These results indicate that IFN-alpha/beta may play an important role in immunologically mediated enteropathies by virtue of its ability to activate NK cells.

摘要

我们研究了α/β干扰素(IFN-α/β)和IFN依赖性效应细胞在小鼠肠道病变形成中的作用。IFN诱导剂聚肌苷酸:聚胞苷酸(poly I:C)增强了新生(CBA×BALB/c)F1小鼠移植物抗宿主反应(GVHR)中自然杀伤(NK)细胞的正常活化,并加剧了GVHR的全身和肠道后果。当给予正常小鼠时,poly I:C本身也产生了类似的肠道病理模式。单次注射纯化的IFN-α/β可重现poly I:C对正常小鼠NK细胞活性和肠道结构的影响,并且通过用抗唾液酸GM1体内清除NK细胞可预防IFN-α/β引起的肠道病变。这些结果表明,IFN-α/β可能因其激活NK细胞的能力而在免疫介导的肠道病变中起重要作用。

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