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Dexamethasone treatment of 3B4.15 T hybridoma cells


ABSTRACT: Investigation of whole genome gene expression level changes in Mus musculus 3B4.15 T hybridoma cells treated with 1microMolar Dexamethasone compared to mock treated cells. Interleukin-7 receptor alpha (IL-7Rα) is essential for T cell survival and differentiation. Glucocorticoids are potent enhancers of IL-7Rα expression with diverse roles in T cell biology. Here we identify the transcriptional repressor, Growth factor independent-1 (Gfi1), as a novel intermediary in glucocorticoid-induced IL-7Rα upregulation. We found Gfi1 to be a major inhibitory target of dexamethasone by microarray expression profiling of 3B4.15 T-hybridoma cells. Concordantly, retroviral transduction of Gfi1 significantly blunted IL-7Rα upregulation by dexamethasone. To further assess the role of Gfi1 in vivo, we generated bacterial artificial chromosome (BAC) transgenic mice, in which a modified Il7r locus expresses GFP to report Il7r gene transcription. By introducing this BAC reporter transgene into either Gfi1-deficient or Gfi1-transgenic mice, we document in vivo that IL-7Rα transcription is upregulated in the absence of Gfi1 and downregulated when Gfi1 is overexpressed. Strikingly, the in vivo regulatory role of Gfi1 was specific for CD8+, and not CD4+ T cells or immature thymocytes. These results identify Gfi1 as a specific transcriptional repressor of the Il7r gene in CD8 T lymphocytes in vivo. A six chip study using total RNA recovered from three separate flasks of mock treated 3B4.15 cells and three separate flasks of Dexamethasone treated 3B4.15 cells . Each chip measures the expression level of 44170 target genes

ORGANISM(S): Mus musculus

SUBMITTER: Batu Erman 

PROVIDER: E-GEOD-39296 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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