ArticleJournal of immunology research2014
OCH ameliorates bone marrow failure in mice via downregulation of T-bet expression.
Article in Journal of immunology research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- [When is there an indication for treatment of isolated leukopenia in SLE and how should it be treated?]Zeitschrift fur Rheumatologie · 2025Article
- Clinicopathological characteristics and prognosis of lupus nephritis patients with positive anti-ribonucleoprotein antibodies.Journal of nephrology · 2025Article
- Platelets and Regulatory T Cells May Induce a Type 2 Immunity That Is Conducive to the Progression and Fibrogenesis of Endometriosis.Frontiers in immunology · 2020Article
- OCH-mediated shift of Th1 and Th2 cytokines by NKT cells in mice with aplastic anemia.Medical oncology (Northwood, London, England) · 2015Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of this study is to evaluate the immune mechanism of OCH in the treatment of AA (also named bone marrow failure, BMF) induced in mice. OCH at a dose of 400 μg/kg was injected intraperitoneally (I.P.) prior to the induction of BMF. Our study showed that the incidence of BMF was 100% in BMF group and 13% in OCH treatment group. Significant higher level of IL-4 and lower level of IFN-γ were observed in OCH group than that in BMF group (P < 0.05) as well as untreated group over BMF (P < 0.05). However, there was no significant difference between OCH and untreated group. Compared with untreated, the expression level of T-bet in OCH and BMF was all significantly higher. However, T-bet expression level was lower in OCH than in BMF. In addition, OCH treatment increased NKT cell fractions of bone marrow and the colonies of CFU-GM. In conclusion, treatment of OCH prior to the induction of BMF could prevent the incidence of BMF possibly through downregulating T-bet expression leading to the transition of immune response from Th1 to Th2, suggesting OCH might be a new therapeutic approach in the treatment of BMF or AA.
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