Neutralization of interferon-gamma in neonatal SOCS1(-/-) mice prevents fatty degeneration of the liver but not subsequent fatal inflammatory disease
Details
Publication Year 2001-09,Volume 104,Issue #1,Page 92-98
Journal Title
IMMUNOLOGY
Publication Type
Journal Article
Abstract
Mice lacking the suppressor of cytokine signalling-1 (SOCS1) die within weeks of birth with extensive fatty degeneration of the liver, consistent with acute hepatic toxicity to interferon-gamma (IFN-gamma), and inflammation of multiple organs. We show here that treatment for 1 week from birth with neutralizing antibody to IFN-gamma rescues SOCS1(-/-) mice from lethal liver disease but the mice subsequently succumb to chronic inflammatory lesions characterized by T-lymphocyte infiltration of skeletal muscle, pancreas, lung, liver and skin. Elevated blood levels of eosinophils, neutrophils and platelets were also observed and the thymic lymphocyte population was depleted of CD4(+) CD8(+) T cells and showed a reduced CD4: CD8 ratio. All T-cell populations in thymus, spleen and lymph node exhibited an increased proportion of cells bearing the activation marker CD44. These data suggest an important role for SOCS1 in T-lymphocyte regulation.
Publisher
BLACKWELL SCIENCE LTD
Keywords
CYTOKINE; INHIBITOR; PROTEIN; LACKING
Terms of Use/Rights Notice
Refer to copyright notice on published article.


Creation Date: 2001-09-01 12:00:00
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