ENAapplication/xmlftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR254/038/SRR25430638/SRR25430638_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR254/042/SRR25430642/SRR25430642_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR254/037/SRR25430637/SRR25430637_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR254/036/SRR25430636/SRR25430636_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR254/039/SRR25430639/SRR25430639_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR254/043/SRR25430643/SRR25430643_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR254/036/SRR25430636/SRR25430636_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR254/039/SRR25430639/SRR25430639_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR254/040/SRR25430640/SRR25430640_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR254/042/SRR25430642/SRR25430642_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR254/041/SRR25430641/SRR25430641_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR254/040/SRR25430640/SRR25430640_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR254/043/SRR25430643/SRR25430643_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR254/041/SRR25430641/SRR25430641_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR254/038/SRR25430638/SRR25430638_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR254/037/SRR25430637/SRR25430637_1.fastq.gzprimary200OKGenomicsJiahuai Han Lab, School of Life Sciences, Xiamen Universityhttps://www.ebi.ac.uk/ena/browser/view/PRJNA998874Mus musculusp38 MAPK is activated during CD8+ T cell primary response. p38 activation promotes effector CD8+ T cell terminal differentiation but represses MPEC formation. p38α/beta deficient mice possess a similar number of virus-specific effector CD8+ T cells as wildtype counterparts. Meanwhile p38α/beta deletion doesn’t influence the clearance of LCMV although it impairs the cytolytic activity of CD8+ T cells. Loss of p38α/beta significantly enhances IL-2-producing Tcm accumulation in mouse spleen with no impact on total memory CD8+ T cell numbers yet. And in line with this, more robust proliferation of memory CD8+ T cells in the secondary response and stronger antigen-specific killing ability in rechallenged mice are resulted from p38α/beta deficiency. These results establish a pivotal role for p38α/beta in skewing MPEC formation toward SLEC differentiation, as well as in suppressing Tcm formation, and thus affecting the recall response. Overall design: To investigate the cooperative function of p38α and p38beta in effector CD8+ T cell differentiation, we immunized p38αfl/flp38betafl/fl and p38αfl/flp38betafl/flGzmBcre mice with LCMV. At 8th day, splenic Db-GP33-41-tetramer+ CD8+ T cells were sorted by flowcytometry. We then performed gene expression profiling analysis using data obtained from RNA-seq of 8 different mice. Comparative gene expression profiling analysis of RNA-seq data for WT cells and its KO counterparts (p38α-/-p38beta-/-).ENAfalseEffect of depletion of p38α and p38beta on gene expression in primary effector CD8+ T cellsEffect of depletion of p38α and p38beta on gene expression in primary effector CD8+ T cells2025-09-242023-08-02PRJNA998874GSE23934810090