Project description:We found that Hopx is required for the function of DC-induced regulatory T cells in vivo. We used microarrays to identify relevant Hopx-targets in such cells after antigenic re-challenge in vivo. CD25/Foxp3 double positive DC-induced Hopx-deficient and sufficient regulatory T cells were FACS sorted to high purity
Project description:Hopx appears to be needed for persistence of Th1 effector memory cells. IFN-gamma-producing Th cells are significantly reduced in Hopx-deficient mice compared to Hopx-expressing littermates and Hopx-deficient Th1 cells show a defective persistence upon adoptive transfer. Moreover, Hopx protects Th1 cells from Fas-mediated cell death in vitro. To further dissect the role of Hopx and to identify target genes of Hopx, we have performed transcriptome analysis to compare gene expression in Hopx-deficient versus Hopx-competent Th1 cells. In agreement with the role of Hopx in supporting survival of Th1 effector memory cells, anti-apoptotic cells were up-regulated and pro-apoptotic genes were down-regulated in Hopx-competent compared to Hopx-deficient Th1 cells.
Project description:We generated Hopx conditional knockout mouse (Hopx-/-) and studied the biological effects of Hopx knockout on the hematopoietic system, via whole-transcriptome RNA-seq. The findigns of our studies support crucial roles of Hopx in physiological and malignant hematopoiesis.