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Pbx1-d Induces T cell Activation and a Decreased Apoptosis in Response to Retinoic Acids (RA)

ABSTRACT: The hypothesis was tested that the Pbx1-d isoform was responsible for the Sle1a.1 phenotypes in CD4+ T cells. Jurkat T cells were transfected with a lentiviral construct expressing Pbx1-d-GFP or control RFP. Pbx1-d over-expression reduced the percentage of late apoptotic cells in response to anti-CD3 and anti-CD28 stimulation as compared with control-Lin28-transfected cells. Overall, these data demonstrate that over-expression of Pbx1-d results in an activated/inflammatory phenotype and in a defective response to RA in Jurkat T cells, strongly suggesting that the increased expression of Pbx1-d is responsible for the Sle1a.1 phenotypes. Jurkat T cells (5 x 105 cells/ml) were transfected with an lentiviral (LV) vector expressing either control (RFP or Lin28) or Pbx1-d-GFP. Total RNA was extracted from GFP+ or RFP+ FACS-sorted Jurkat T cells transfected LV-GFP-Pbx1-d or LV-RFP, as well as non-transfected cells in 4 independent transfections per group.

ORGANISM(S): Homo sapiens

SUBMITTER: Igor Dozmorov

PROVIDER: E-GEOD-22799 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Pbx1-d Induces T cell Activation and a Decreased Apoptosis in Response to Retinoic Acids (RA)

Project description:The hypothesis was tested that the Pbx1-d isoform was responsible for the Sle1a.1 phenotypes in CD4+ T cells. Jurkat T cells were transfected with a lentiviral construct expressing Pbx1-d-GFP or control RFP. Pbx1-d over-expression reduced the percentage of late apoptotic cells in response to anti-CD3 and anti-CD28 stimulation as compared with control-Lin28-transfected cells. Overall, these data demonstrate that over-expression of Pbx1-d results in an activated/inflammatory phenotype and in a defective response to RA in Jurkat T cells, strongly suggesting that the increased expression of Pbx1-d is responsible for the Sle1a.1 phenotypes.

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