生物
内部收益率1
淋巴细胞生成
干扰素调节因子
淋巴细胞性脉络膜脑膜炎
造血
胸腺细胞
干扰素
IRF8
CD8型
骨髓生成
病毒学
免疫学
转录因子
分子生物学
干细胞
癌症研究
基因
细胞生物学
抗原
免疫系统
先天免疫系统
遗传学
作者
Tomohiro Matsuyama,Tohru Kimura,Motoo Kitagawa,Klaus Pfeffer,Toshifumi Kawakami,Nobumasa Watanabe,Thomas M. Kündig,Ryuichi Amakawa,Kenji Kishihara,Andrew Wakeham,Julia M. Potter,Caren Furlonger,A. Narendran,Haruhiko Suzuki,Pamela S. Ohashi,Christopher J. Paige,Tadatsugu Taniguchi,Tak W. Mak
出处
期刊:Cell
[Elsevier]
日期:1993-10-01
卷期号:75 (1): 83-97
被引量:571
标识
DOI:10.1016/s0092-8674(05)80086-8
摘要
Interferon regulatory factor 1 (IRF-1), a transcriptional activator, and its antagonistic repressor, IRF-2, were originally identified as regulators of the type I interferon (IFN) system. We have generated mice deficient in either IRF-1 or IRF-2 by gene targeting in embryonic stem cells. IRF-1-deficient fibroblasts lacked the normally observed type I IFN induction by poly(I):poly(C), while they induced type I IFN to similar levels as the wild type following Newcastle disease virus (NDV) infection. In contrast, IRF-2-deficient fibroblasts showed up-regulated type I IFN induction by NDV infection. A profound reduction of TCR alpha beta+CD4-CD8+ T cells in IRF-1-deficient mice, with a thymocyte developmental defect, reveals a critical role for IRF-1 in T cell development. IRF-2-deficient mice exhibited bone marrow suppression of hematopoiesis and B lymphopoiesis and mortality following lymphocytic choriomeningitis virus infection.
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