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Here, we show that C\u03b31Cre-mediated deletion of Eif3e, which encodes a subunit of the eIF3 translation initiation complex, in B cells causes lymphoproliferation, malignant transformation of Eif3e-sufficient bystander lymphocytes, and premature death. Eif3e-deficient B cells upregulate the costimulatory molecule CD80, promoting CD4+ T cell activation and differentiation into IL-4\u2013producing TFH-like cells. These cells, in turn, activate bystander B cells, increase MHC class II expression, and establish a feedforward loop of Eif3e deletion and lymphocyte activation. Despite their hyperactivated state, Eif3e-deficient B cells exhibit impaired proliferation, reduced survival, and defective differentiation. This self-amplifying circuit of aberrant B and T cell activation ultimately drives malignant transformation of Eif3e-sufficient lymphocytes. Our findings uncover an eIF3e-dependent translational checkpoint that preserves immune homeostasis and restrains lymphomagenesis.<\/jats:p>","DOI":"10.1084\/jem.20251968","type":"journal-article","created":{"date-parts":[[2026,5,14]],"date-time":"2026-05-14T06:21:03Z","timestamp":1778739663000},"update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":3,"title":["eIF3e-mediated translational checkpoint maintains immune tolerance and prevents lymphoid malignancy"],"prefix":"10.1084","volume":"223","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3418-6291","authenticated-orcid":true,"given":"Lianghua","family":"Lin","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00mcjh785","id-type":"ROR","asserted-by":"publisher"}],"name":"State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Faculty of Medicine and Life Sciences, Xiamen University 1 , 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