ArticleHepatology international2010
Opposite effects of high and low doses of interleukin-2 on T cell-mediated hepatitis in mice (interleukin-2 on hepatitis).
Article in Hepatology international, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Article
- Human CD39Cellular & molecular immunology · 2017Article
- Enhanced hepatotoxicity by acetaminophen in Vanin-1 knockout mice is associated with deficient proliferative and immune responses.Biochimica et biophysica acta · 2016Article
- Ghrelin reduces liver impairment in a model of concanavalin A-induced acute hepatitis in mice.Drug design, development and therapy · 2015Article
- 15-Deoxy- γ 12,14-prostaglandin J2 Reduces Liver Impairment in a Model of ConA-Induced Acute Hepatic Inflammation by Activation of PPAR γ and Reduction in NF- κ B Activity.PPAR research · 2014Article
- Ethyl pyruvate pretreatment attenuates concanavalin a-induced autoimmune hepatitis in mice.PloS one · 2014Article
- Immune mechanisms of Concanavalin A model of autoimmune hepatitis.World journal of gastroenterology · 2012Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeConcanavalin A (Con A)-induced hepatitis is an extensively used animal model of T cell-mediated acute hepatitis. A variety of cytokines, including interleukin 4 (IL-4), interferon gamma (IFN-γ), and tumor necrosis factor alpha (TNF-α), have been shown to play important roles in Con A-induced liver injury. However, the role of IL-2, a critical cytokine in the development and function of T cells and a clinical therapeutics for virus infection and tumor, has not been carefully examined in this model.
methodsIn this study, we investigated the function of IL-2 in Con A-induced hepatitis by using various strategies of rhIL-2 pretreatment. We treated mice with two rhIL-2 administration strategies: a single injection of high dose of rhIL-2 (IL-2(hi), 50 × 10(3) U/mouse) and four injections of low dose of rhIL-2 (IL-2(4lo), 5 × 10(3) U/mouse).
resultsIL-2(hi) pretreatment ameliorated Con A-induced liver injury, while IL-2(4lo) aggravated Con A-induced liver injury. IL-2(hi) pretreatment reduced Con A-induced elevation of serum TNF-α while IL-2(4lo) pretreatment did not. Serum IL-4 and TNF-α were high 6 h after Con A injection in IL-2(4lo) mice, while it was undetectable in IL-2(hi) and non-pretreated mice. IL-2(hi) pretreatment reduced Con A-induced accumulation of T cells in liver while IL-2(4lo) pretreatment increased accumulation of NK cells.
conclusionVarious strategies of rhIL-2 administration play different roles in Con A-induced hepatitis, suggesting the importance of IL-2 administrative regime in clinical liver diseases.
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