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Type I Natural Killer T (iNKT) Cells Regulate Inflammatory Immune Response in Mice Liver Injury Induced by CCl4
Author(s) -
PARK OGYI,
JEONG WONIL,
GAO BIN
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1072.16
Subject(s) - natural killer t cell , liver injury , ccl4 , proinflammatory cytokine , immune system , immunology , natural killer cell , tumor necrosis factor alpha , biology , medicine , inflammation , carbon tetrachloride , t cell , chemistry , endocrinology , cytotoxic t cell , biochemistry , organic chemistry , in vitro
Natural killer T (NKT) cells are the predominant lymphocyte population (up to 30 %) in the mouse liver and play an important role in Concanavalin A (Con A) and α‐Galactosylceramide (α‐GalCer) induced liver injury by producing inflammatory cytokines, such as IFN‐γ and TNF‐α and activating other cell populations including NK and T cells. In this study, we examined the role of NKT cells in carbon tetrachloride (CCl4) liver injury using type I, or invariant NKT (iNKT) KO mice (Ja18−/−) and WT C57BL/6 mice. Liver injury in mice was induced by intraperitoneal single injection of 1 ml/kg body weight of 10% CCl4 and samples were collected at different time points. The administration of CCl4 to mice induced liver injury with depletion of NKT cells and elevation of NK cells in the liver in both mice groups. Compared to WT mice, Jα 18−/− mice showed severe liver damage and increased neutrophil infiltration at early time point. Serum levels of inflammatory cytokines, such as TNF‐α, MCP‐1, IL‐4 and IL‐6, as well as mRNA expression were remarkably increased in Jα18−/− mice after CCl4 administration compared to WT mice. These findings suggest that type I NKT cells may protect against inflammatory immune response via suppressing the production of proinflammatory cytokines in early stage liver injury.