| First Author | Lu B | Year | 1998 |
| Journal | Proc Natl Acad Sci U S A | Volume | 95 |
| Issue | 14 | Pages | 8233-8 |
| PubMed ID | 9653170 | Mgi Jnum | J:48016 |
| Mgi Id | MGI:1274996 | Doi | 10.1073/pnas.95.14.8233 |
| Citation | Lu B, et al. (1998) Targeted disruption of the interferon-gamma receptor 2 gene results in severe immune defects in mice. Proc Natl Acad Sci U S A 95(14):8233-8 |
| abstractText | 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. |
