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Here, we show that activation of p38 MAPK during the primary response of CD8+ T cells orchestrates a delicate balance between the formation of short-lived effector cells and memory precursor effector cells. p38\u03b1fl\/flp38\u03b2fl\/flGzmBcre\/\u2212 mice, in which p38\u03b1 and p38\u03b2 were efficiently deleted in CD8+ T cells and also in early stages of T-cell development, were used in studying the role of the p38 pathway in T cells. The deletion of p38\u03b1 and p38\u03b2 (simplified as p38\u03b1\/\u03b2) has very minor effects on thymic and peripheral T-cell development. In contrast, p38\u03b1\/\u03b2-deficient CD8+ T cells were skewed toward a central memory phenotype and mounted stronger recall responses upon secondary challenge. Transcriptomic analyses of antigen-specific CD8+ T cells revealed that p38\u03b1\/\u03b2 deficiency is associated with reduced effector gene expression and enhanced memory-associated programs. Furthermore, in vitro differentiated p38\u03b1\/\u03b2-deficient CD8+ T cells showed superior persistence and functional responses after adoptive transfer. These results establish a role for p38 in controlling effector CD8+ T-cell differentiation and memory formation, and reinforce the therapeutic potential of targeting this pathway, aligning with recent studies demonstrating the beneficial effects of p38 inhibitors in adoptive cell therapy.<\/jats:p>","DOI":"10.1093\/jimmun\/vkaf214","type":"journal-article","created":{"date-parts":[[2025,10,10]],"date-time":"2025-10-10T17:33:03Z","timestamp":1760117583000},"page":"3357-3373","source":"Crossref","is-referenced-by-count":1,"title":["p38 signaling enhances short-lived effector cell differentiation and weakens central memory CD8+ T-cell formation"],"prefix":"10.1093","volume":"214","author":[{"given":"Lichen","family":"Hu","sequence":"first","affiliation":[{"name":"State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Faculty of Medicine and Life Sciences, Xiamen University , 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