Effect of depletion of p38α and p38beta on gene expression in primary effector CD8+ T cells

p38 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. 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-/-).