Targeted disruption of IRF-1 or IRF-2 results in abnormal type I IFN gene induction and aberrant lymphocyte development
作者： Toshifumi Matsuyama , Tohru Kimura , Motoo Kitagawa , Klaus Pfeffer , Takatoshi Kawakami
DOI: 10.1016/S0092-8674(05)80086-8
关键词:
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 embryonic stem cells. IRF-1-deficient fibroblasts lacked normally observed IFN induction poly(I):poly(C), while they induced to similar levels wild following Newcastle disease virus (NDV) infection. In contrast, IRF-2-deficient showed up-regulated NDV A profound reduction TCR alpha beta+CD4-CD8+ T cells mice, with thymocyte developmental defect, reveals critical role for cell development. exhibited bone marrow suppression hematopoiesis B lymphopoiesis mortality lymphocytic choriomeningitis
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