To study the role of the interferon- (IFN) γR2 chain in IFN-γ signaling and immune function, IFN-γR2-deficient mice have been generated and characterized. Cells derived from IFN-γR2 -/- mice are unable to activate either JAK/STAT signaling proteins or gene transcription in response to IFN-γ. The lack of IFN-γ responsiveness alters IFN-γ-induced Ig class switching by B cells from these mice. In vitro cultures of T cells demonstrate that the T cells from the IFN-γR2 -/- mice have a defect in Th1 cell differentiation. The IFN-γR2 (-/-) mice also produce lower amounts of IFN-γ in response to antigenic challenge. In addition, IFN-γR2 -/- mice are defective in contact hypersensitivity and are highly susceptible to infection by Listeria monocytogenes. These results demonstrate that the IFN-γR2 is essential for IFN-γ-mediated immune responses in vivo.
|Original language||English (US)|
|Number of pages||6|
|Journal||Proceedings of the National Academy of Sciences of the United States of America|
|State||Published - Jul 7 1998|
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