Effect of depletion of p38α and p38β on gene expression in naïve 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/β-deficient mice possess a similar number of virus-specific effector CD8+ T cells as wildtype counterparts. Meanwhile p38α/β deletion doesn’t influence the clearance of LCMV although it impairs the cytolytic activity of CD8+ T cells. Loss of p38α/β 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/β deficiency. These results establish a pivotal role for p38α/β in skewing MPEC formation toward SLEC differentiation, as well as in suppressing Tcm formation, and thus affecting the recall response. p38α was reported to be essential in CD8+ T cell maturation, and our mice were observed to be at loss of p38α/β expression in thymic T cells during development. So it's important to see the influence of p38α/β deletion on peripheral naive CD8+ T cells and its potential inborn impact on later events. This would help determining the exact role of p38 signaling in CD8+ T cell immune responses.