期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：1998
卷号：95
期号：14
页码：8233-8238
DOI：10.1073/pnas.95.14.8233
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：To study the role of the interferon- (IFN) {gamma}R2 chain in IFN-{gamma} signaling and 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.
