ArticleMedical oncology (Northwood, London, England)2015
OCH-mediated shift of Th1 and Th2 cytokines by NKT cells in mice with aplastic anemia.
Article in Medical oncology (Northwood, London, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed, 6 citations in OpenAlex.
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6 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The immune-mediated destruction of bone marrow (BM) is the major cause of aplastic anemia (AA) in most patients. It has been shown that an imbalance of Th1 and Th2 cells is involved in immune-mediated destruction of BM in patients with AA. In the present study, we determined the role of NKT cells in regulating the balance of Th1 and Th2 cytokines. We found that the number of NKT cells from bone marrow mononuclear cells was lower in AA mice than normal mice. When treated with α-GalCer or its analog OCH, AA mice showed a significantly reduced capacity of NKT cell expansion. Furthermore, we found that the number of IFN-γ-producing NKT cells was higher in AA mice compared to normal counter-partners. However, OCH treatment inhibited IFN-γ production and enhanced IL-4 production by NKT cells in which we saw a balanced Th1- to Th2-type cytokines in AA mice. Interestingly, we observed that OCH treatment promoted hematopoietic cell growth, as indicated by increased colony counts in AA mice. Taken together, our results not only demonstrated a role of OCH in the maintenance of Th1/Th2 balance and recovery of hematopoietic cell growth, but also revealed a therapeutic potential of OCH in AA.
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