Lu B, Ebensperger C, Dembic Z, Wang Y, Kvatyuk M, Lu T, Coffman R L, Pestka S, Rothman P B
Integrated Program of Molecular, Cellular, and Biophysical Studies, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.
Proc Natl Acad Sci U S A. 1998 Jul 7;95(14):8233-8. doi: 10.1073/pnas.95.14.8233.
To study the role of the interferon- (IFN) gammaR2 chain in IFN-gamma signaling and immune function, IFN-gammaR2-deficient mice have been generated and characterized. Cells derived from IFN-gammaR2 -/- 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-gammaR2 -/- mice have a defect in Th1 cell differentiation. The IFN-gammaR2 (-/-) mice also produce lower amounts of IFN-gamma in response to antigenic challenge. In addition, IFN-gammaR2 -/- mice are defective in contact hypersensitivity and are highly susceptible to infection by Listeria monocytogenes. These results demonstrate that the IFN-gammaR2 is essential for IFN-gamma-mediated immune responses in vivo.
为了研究干扰素-γ（IFN-γ）受体2链在IFN-γ信号传导和免疫功能中的作用，已培育并鉴定出IFN-γ受体2缺陷型小鼠。源自IFN-γ受体2 -/-小鼠的细胞无法响应IFN-γ激活JAK/STAT信号蛋白或基因转录。IFN-γ反应性的缺乏改变了这些小鼠B细胞中IFN-γ诱导的Ig类别转换。T细胞的体外培养表明，来自IFN-γ受体2 -/-小鼠的T细胞在Th1细胞分化方面存在缺陷。IFN-γ受体2 (-/-)小鼠对抗抗原刺激产生的IFN-γ量也较低。此外，IFN-γ受体2 -/-小鼠在接触性超敏反应方面存在缺陷，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受体2对于体内IFN-γ介导的免疫反应至关重要。
