期刊
IMMUNOLOGY
卷 104, 期 1, 页码 92-98出版社
BLACKWELL SCIENCE LTD
DOI: 10.1046/j.1365-2567.2001.01294.x
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资金
- NCI NIH HHS [R01 CA022556, R37 CA022556, CA-22556] Funding Source: Medline
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.
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