AbstractImmunoproteasomes containing the IFN‐inducible subunits β1i (LMP2), β2i (MECL‐1) and β5i (LMP7) alter proteasomal cleavage preference and optimize the generation of peptide ligands of MHC class I molecules. Here, we report on an unexpected new function of immunoproteasome subunits for the survival and expansion of CD4+ and CD8+ T cells during viral infection of mice. The effect of immunoproteasome subunit deficiency on T‐cell survival upon adoptive transfer was most prominent for the lack of LMP7 followed by MECL‐1 and LMP2. The survival of T cells in uninfected mice or the homeostatic expansion after transfer into RAG‐2−/− mice was not affected by the lack of the immunosubunits. Lymphocytic choriomeningitis virus (LCMV)‐specific CD8+ T cells lacking LMP7 or MECL‐1 started to divide after transfer into LCMV‐infected mice but experienced a considerable cell loss within 2 days after transfer. We provide strong evidence that the loss of immunoproteasome‐deficient T cells after transfer is not a consequence of graft rejection by the host, but instead is based on the requirement for immunoproteasomes for the survival of T cells in LCMV‐infected mice. Therefore, the immunoproteasome may qualify as a potential new target for the suppression of undesired proinflammatory T‐cell responses.