Polycystic kidneys and chronic inflammatory lesions are the delayed consequences of loss of the suppressor of cytokine signaling-1 (SOCS-1)

Abstract

Mice with inactivation of the gene encoding the suppressor of cytokine signaling-1 (SOCS-1) die in neonatal life with an IFN-γdependent inflammatory disease dominated by fatty degeneration and necrosis of the liver. To establish the long-term pathological consequences of loss of SOCS-1 in mice, where initial survival was made possible by also deleting the IFN-γ gene, a comparison was made of the lifespan of groups of SOCS-1-1- IFN-γ-1-, SOCS-1+1+ IFN-γ-1- and SOCS-1+1+ IFN-γ+1+ mice. Mice lacking the genes for both SOCS-1 and IFN-γ exhibited an accelerated death rate compared with control groups. Disease states developing selectively in SOCS-1-1- IFN-γ-1- mice were polycystic kidneys, pneumo..