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- W70307114 abstract "Abstract Ikaros is a transcription factor that is expressed almost exclusively in cells of the hematopoietic lineage. Ikaros null mice lack several hematopoietic cell lineages including some dendritic cell (DC) subsets. Additionally, several Ikaros null bone marrow (BM) progenitor populations have a decreased expression of the receptor tyrosine kinase, Flt3. DCs can be generated in vitro by culture of BM with either GM-CSF or Flt3L (the ligand for Flt3). Our studies find that loss of Ikaros leads to a specific defect in the ability of BM precursors to generate DCs in response to culture with Flt3L but not in response to culture with GM-CSF. Those DCs that do develop from the culture of Ikaros null BM with Flt3L have an activated phenotype with higher expression of MHC class II and the costimulatory molecules CD40, CD80 and CD86 than their wild type counterparts. An examination of gene expression in Ikaros null BM progenitors cultured with Flt3L shows an inappropriately low expression of Irf4, Irf8 and Spib, genes encoding transcription factors known to be important for DC development. Studies are currently underway to determine whether enforced expression of Ikaros, Flt3 or one of the above-mentioned transcription factors can rescue DC development upon culture of Ikaros null BM with Flt3L. These studies will provide a potential molecular mechanism for the impaired development of DCs in Ikaros null mice." @default.
- W70307114 created "2016-06-24" @default.
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- W70307114 date "2010-04-01" @default.
- W70307114 modified "2023-09-24" @default.
- W70307114 title "Ikaros null mice demonstrate defects in dendritic cell development. (36.17)" @default.
- W70307114 doi "https://doi.org/10.4049/jimmunol.184.supp.36.17" @default.
- W70307114 hasPublicationYear "2010" @default.
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