Measles continues to be an important cause of childhood mortality in developing countries. Measles virus (MV) is lymphotropic and infects high percentages of B‐ and T‐lymphocytes in lymphoid tissues. Cellular immunity is considered crucial for viral clearance; however, MV‐specific T‐lymphocytes generated during primary infection also constitute a potential target for MV infection. We therefore aimed to identify T‐lymphocyte subsets that can clear MV infection without becoming infected. To this end, we infected human EBV transformed B‐lymphoblastic cell lines (B‐LCL) with a recombinant MV strain expressing enhanced GFP, and co‐cultured these with non‐infected B‐LCL resulting in rapid viral spread. MV‐specific CD8+ T‐cell clones efficiently suppressed MV dissemination in autologous and HLA‐matched, but not in HLA‐mismatched B‐LCL. In contrast, CD4+ T‐cell clones could not control MV dissemination but became a target for MV infection themselves. Furthermore, PBMC collected 6–9 months after acute measles and stimulated with autologous MV‐infected B‐LCL also efficiently suppressed MV dissemination; this was mediated by the fraction containing CD8+ T‐lymphocytes. In conclusion, we have developed a powerful tool to study cellular immunity against measles, and demonstrate that control of MV dissemination is mediated by virus‐specific CD8+ rather than by CD4+ T‐lymphocytes.