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JunB is required for expression of genes controlled by BATF and IRF4 in CD4+ T cell responses, but the role of JunB in CD8+ T cells remains unknown. Here, we demonstrate that JunB is essential for cytotoxic CD8+ T cell responses. JunB expression is transiently induced, depending on the T cell receptor signal strength. JunB deficiency severely impairs the clonal expansion of effector CD8+ T cells in response to acute infection with Listeria monocytogenes. Junb-deficient CD8+ T cells fail to control transcription and chromatin accessibility of a specific set of genes regulated by BATF and IRF4, resulting in impaired cell survival, glycolysis, and cytotoxic CD8+ T cell differentiation. Furthermore, JunB deficiency enhances the expression of co-inhibitory receptors, including programmed cell death 1 (PD-1) and T cell immunoglobulin mucin-3 (TIM3) upon activation of naive CD8+ T cells. These results indicate that JunB, in collaboration with BATF and IRF4, promotes multiple key events in the early stage of cytotoxic CD8+ T cell responses.<\/jats:p>","DOI":"10.1093\/intimm\/dxae063","type":"journal-article","created":{"date-parts":[[2024,10,19]],"date-time":"2024-10-19T18:15:22Z","timestamp":1729361722000},"page":"203-220","source":"Crossref","is-referenced-by-count":7,"title":["JunB is required for CD8+ T cell responses to acute infections"],"prefix":"10.1093","volume":"37","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6804-0629","authenticated-orcid":false,"given":"Shukla","family":"Sarkar","sequence":"first","affiliation":[{"name":"Immune Signal Unit, Okinawa Institute of Science and Technology, Graduate University (OIST) , Onna-son, Okinawa 904-0495 ,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Naoyuki","family":"Taira","sequence":"additional","affiliation":[{"name":"Immune Signal Unit, Okinawa Institute of Science and 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