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RNA-seq analysis of old versus young, male versus female, and naïve versus effector memory CD4+ T cells.

ABSTRACT: RNA-seq analysis of old versus young, male versus female, and naïve versus effector memory CD4+ T cells.

PROVIDER: PRJNA764770 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15988150.fastq.gz	Fastqsanger.gz
	SRR15988151.fastq.gz	Fastqsanger.gz
	SRR15988152.fastq.gz	Fastqsanger.gz
	SRR15988153.fastq.gz	Fastqsanger.gz
	SRR15988154.fastq.gz	Fastqsanger.gz

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RNA-seq analysis of old versus young, male versus female, and naïve versus effector memory CD4+ T cells.

Project description:Impaired T cell immunity in the elderly increases mortality from infectious disease. The branching of Asparagine-linked glycans is a critical negative regulator of T cell immunity. We found that N-glycan branching increases with age in female > male, naïve > memory and CD4+ > CD8+ T cells, likely contributing to immunosenescence. To investigate the mechanisms driving these changes, we performed RNA-seq analysis on highly purified young and old naive (CD3+CD4+CD25-CD62L+CD44-) and effector memory (CD3+CD4+CD25-CD62L-CD44+) CD4+ T cells from male and female mice. Comparing young and old CD4+ TN cells, 158 and 192 differentially expressed genes (DEGs) were identified in females and males, respectively. Remarkably, only 44 of these overlapped between the sexes. There were no significant differences in gene expression of N-glycan branching enzymes or other relevant glycosylation genes. Among the 114 DEGs in female but not male CD4+ TN cells, four were within the IL-7 signaling pathway, a pathway previously implicated in regulating N-glycan branching. This included reduced expression of IL7Rα (CD127) and increased expression of Suppressor of cytokine signaling 1 (Socs1), Socs3, and Janus kinase 3 (Jak3). Other IL-7 signaling pathway genes were unchanged.

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Phosphatidylinositol-3-kinase p110 delta differentially restrains and directs naïve versus effector CD8+ T cell transcriptional programs Phosphatidylinositol-3-kinase p110 delta differentially restrains and directs naïve versus effector CD8+ T cell transcriptional programs

Project description:Phosphatidylinositol-3-kinase p110 delta (PI3Kp110δ) is pivotal for CD8+ T cell immune responses. To inform how PI3Kp110δ regulates CD8+ T cells, the current study focuses on PI3Kp110δ controlled transcriptional programs and reveals how PI3Kp110δ selectively induces and represses expression of key genes that create a cytotoxic T cell (CTL). The data identify differences in PI3Kp110δ regulated transcriptional programs between naïve and cytotoxic T cells including differential control of cytolytic effector molecules, costimulatory receptors and the critical inhibitory receptors CTLA4 and SLAMF6. However, common to both naïve and effector cells is PI3Kp110δ control of the production of chemokines and cytokines that orchestrate communication between the adaptive and innate immune system. The study provides a comprehensive resource for understanding how PI3Kp110δ uses multiple mechanisms dependent on Protein Kinase B/AKT, FOXO1 dependent and independent mechanisms and mitogen-activated protein kinases (MAPK) to direct CD8+ T cell fate.

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