ArticleAmerican journal of hematology2009
Altered cytokine profiles in patients with Chuvash polycythemia.
Article in American journal of hematology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- The von Hippel-Lindau Chuvash mutation in mice alters cardiac substrate and high-energy phosphate metabolism.American journal of physiology. Heart and circulatory physiology · 2016Article
- Oxygen-dependent Regulation of Erythropoietin Receptor Turnover and Signaling.The Journal of biological chemistry · 2016Article
- Pathogenesis of Myeloproliferative Neoplasms: Role and Mechanisms of Chronic Inflammation.Mediators of inflammation · 2015Review
- Iron deficiency modifies gene expression variation induced by augmented hypoxia sensing.Blood cells, molecules & diseases · 2014Article
- Hypoxia-inducible factors enhance the effector responses of CD8(+) T cells to persistent antigen.Nature immunology · 2013Article
- Regulation of erythropoiesis by hypoxia-inducible factors.Blood reviews · 2013Review
- Chuvash polycythemia VHLR200W mutation is associated with down-regulation of hepcidin expression.Blood · 2011Article
- The heterozygote advantage of the Chuvash polycythemia VHLR200W mutation may be protection against anemia.Haematologica · 2011Article
- Increased size of solid organs in patients with Chuvash polycythemia and in mice with altered expression of HIF-1alpha and HIF-2alpha.Journal of molecular medicine (Berlin, Germany) · 2010Article
- Review
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Chuvash polycythemia results from a homozygous 598C>T mutation in exon 3 of the von Hippel-Lindau (VHL) gene. This disrupts the normoxia pathway for degrading hypoxia inducible factor (HIF)-1alpha and HIF-2alpha causing altered expression of HIF-1 and HIF-2 inducible genes. As hypoxia induces expression of pro-inflammatory cytokines, we hypothesized that there might be an elevation of Th1 cytokines in the setting of Chuvash polycythemia. We analyzed plasma concentrations of Th1 (interleukins-2 and 12, interferon-gamma, granulocyte-monocyte colony-stimulating factor, tumor necrosis factor-alpha) and Th2 cytokines (interleukins-4, 5, 10, and 13) using the Bio-Plex multiplex suspension array system in 34 VHL598C>T homozygotes and 32 VHL wild-type participants from Chuvashia. Concentrations of all the Th1 and Th2 cytokines measured were elevated in the VHL598C>T homozygotes compared with the control wild-type participants, but the ratios of Th1 to Th2 cytokines did not differ by genotype. In parallel, peripheral blood concentrations of CD4 positive T-helper cells and CD4/CD8 ratio were lower in the VHL598C>T homozygotes. In conclusion, the up-regulated hypoxic response in Chuvash polycythemia is associated with increased plasma products of both the Th1 and Th2 pathways, but the balance between the two pathways seems to be preserved.
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