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- W3135945997 abstract "Patients with myelodysplastic syndromes (MDSs) display severe anemia but the mechanisms underlying this phenotype are incompletely understood. Right open-reading-frame kinase 2 (RIOK2) encodes a protein kinase located at 5q15, a region frequently lost in patients with MDS del(5q). Here we show that hematopoietic cell-specific haploinsufficient deletion of Riok2 (Riok2f/+Vav1cre) led to reduced erythroid precursor frequency leading to anemia. Proteomic analysis of Riok2f/+Vav1cre erythroid precursors suggested immune system activation, and transcriptomic analysis revealed an increase in p53-dependent interleukin (IL)-22 in Riok2f/+Vav1cre CD4+ T cells (TH22). Further, we discovered that the IL-22 receptor, IL-22RA1, was unexpectedly present on erythroid precursors. Blockade of IL-22 signaling alleviated anemia not only in Riok2f/+Vav1cre mice but also in wild-type mice. Serum concentrations of IL-22 were increased in the subset of patients with del(5q) MDS as well as patients with anemia secondary to chronic kidney disease. This work reveals a possible therapeutic opportunity for reversing many stress-induced anemias by targeting IL-22 signaling." @default.
- W3135945997 created "2021-03-29" @default.
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- W3135945997 date "2021-03-22" @default.
- W3135945997 modified "2023-10-17" @default.
- W3135945997 title "Blockade of IL-22 signaling reverses erythroid dysfunction in stress-induced anemias" @default.
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- W3135945997 doi "https://doi.org/10.1038/s41590-021-00895-4" @default.
- W3135945997 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/8026551" @default.
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- W3135945997 hasPublicationYear "2021" @default.
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