Targeted disruption of the interferon-gamma receptor 2 gene results in severe immune defects in mice.

Abstract:

: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.

authors

Lu B,Ebensperger C,Dembic Z,Wang Y,Kvatyuk M,Lu T,Coffman RL,Pestka S,Rothman PB

doi

10.1073/pnas.95.14.8233

subject

Has Abstract

pub_date

1998-07-07 00:00:00

pages

8233-8

issue

14

eissn

0027-8424

issn

1091-6490

journal_volume

95

pub_type

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