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Global gene expression analysis of peripheral blood cells, pluripotent cell lines, and iPS-derived T cells

ABSTRACT: Exhaustion of antigen-specific T cells represents a major challenge to adoptive immunotherapy against many types of cancer and viral infection. In an effort to overcome this problem, we reprogrammed clonally expanded antigen-specific CD8+ T cells from an HIV-1-infected patient to pluripotency. The T cell-derived induced pluripotent stem cells (T-iPSCs) were then redifferentiated into CD8+ T cells that had high proliferative capacity and elongated telomeres. To confirm that T-iPSCs were compatible to other embryonic stem cells (ESCs) but different from T cells, and that redifferentiated T cells were compatible to T cells but different from natural killer (NK) cells, we analyzed and compared the gene expression profiles of the samples by cDNA microarray. These analyses revealed that our T-iPSCs and redifferentiated T cells were essentially the same as their counterpart pluripotent stem cells and T cells, respectively.

ORGANISM(S): Homo sapiens

PROVIDER: GSE43136 | GEO | 2012/12/25

SECONDARY ACCESSION(S): PRJNA184700

REPOSITORIES: GEO

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Project description:Leptin receptors (Lepr) are expressed by various types of stem cells including mesenchymal stem cells, hematopoietic stem cells, embryonic stem cells, and induced pluripotent stem cells. Leptin/lepr signaling is also a central regulator of metabolism. However, the role of Lepr in pluripotency, metabolic disease progression and growth development is still controversial and poorly understood. In the present study, we explored the Lepr function in disease progression, pluripotency and metabolism using day 14.5 mouse embryonic fibroblasts (MEFs) and their reprogrammed induced pluripotent stem cells (iPSCs) as model system. We successfully reprogrammed mouse embryonic fibroblasts into iPSCs from control and db/db (Lepr deficient) mice. Using a global quantitative proteomic approach, we identified key pathways regulating pluripotency, metabolic homeostasis and protein synthesis during fetal growth and development. The Lepr MEFs show abnormal metabolic abnormalities and mitochondrial dysfunction as compared to control MEFs, while Lepr iPSCs show upregulated elongated factor 4 e (eIF4e) protein synthesis pathway and altered Oct4 and Stat3 pathways which are involved in normal fetal growth development. Furthermore, chip analysis revealed that higher Stat3 binding on the promoter of eIF4e in Lepr iPSCs leads to higher protein synthesis in these cell types as compared to control iPSCs. Finally, point mutation corrected Lepr iPSCs using CRISPR/Cas9 gene editing method showed recovered pluripotency, metabolic and protein synthesis pathways. In conclusion, we have shown that Lepr signaling is involved in the regulation of the metabolic properties and key developmental pathways in MEFs and stemness of pluripotent stem cells. Disruption of Lepr signaling has been shown to involve in the pathophysiology of various diseases including obesity and diabetes. The generated MEFs and iPSCs in this present study provide valuable tools to explore the role of Lepr in the progression of obesity, diabetes and metabolic abnormalities, and to find the putative targets of Lepr signaling during the development of these diseases.

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Global gene expression analysis of peripheral blood cells, pluripotent cell lines, and iPS-derived T cells

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