Targeted disruption of the interferon-γ receptor 2 gene results in severe immune defects in mice
Targeted disruption of the interferon-γ receptor 2 gene results in severe immune defects in mice
复制标题
DOI：
10.1073/pnas.95.14.8233
复制
发表时间：
1998-07-07
影响因子：
11.1
通讯作者：
Rothman, PB
中科院分区：
文献类型：
--
作者：
Lu, BF;Ebensperger, C;Rothman, PB
为了研究干扰素-（IFN）γ R2链在IFN-γ信号传导酸性免疫功能中的作用，产生并表征了IFN-γ R2缺陷型小鼠。源自IFN-γ R2 -/-小鼠的细胞不能响应IFN-γ激活JAK/STAT信号传导蛋白或基因转录。IFN-γ反应性的缺乏改变了这些小鼠的B细胞对IFN-γ诱导的IG类转换。T细胞的体外培养证明来自IFN-γ R2 -/-小鼠的T细胞在Th 1细胞分化中具有缺陷。IFN-γ R2（-/-）小鼠在响应抗原攻击时也产生较低量的IFN-γ。此外，IFN-γ R2 -/-小鼠在接触性超敏反应方面有缺陷，并且对单核细胞增生李斯特菌感染高度敏感。这些结果表明，IFN-γ R2对于IFN-γ介导的体内免疫应答是必需的。
To study the role of the interferon- (IFN) gamma R2 chain in IFN-gamma signaling acid immune function, IFN-gamma R2-deficient mice have been generated and characterized. Cells derived from IFN-gamma R2 -/- mice are unable to activate either JAK/STAT signaling proteins or gene transcription in response to IFN-gamma. The lack of IFN-gamma responsiveness alters IFN-gamma-induced Ig class switching by B cells from these mice. In vitro cultures of T cells demonstrate that the T cells from the IFN-gamma R2 -/- mice have a defect in Th1 cell differentiation. The IFN-gamma R2 (-/-) mice also produce lower amounts of IFN-gamma in response to antigenic challenge. In addition, IFN-gamma R2 -/- mice are defective in contact hypersensitivity and are highly susceptible to infection by Listeria monocytogenes. These results demonstrate that the IFN-gamma R2 is essential for IFN-gamma-mediated immune responses in vivo.