Listeria monocytogenes infection of mice leads to a rapid expansion of activated T cells, followed by a decline in specific cells once the bacteria are eliminated. In order to define the relationship between T‐cell proliferation and activation, and to investigate the role of apoptosis in limiting the expansion, the expression of activation markers, uptake of 5‐bromo‐2′‐deoxyuridine (BrdU) in vivo and the incidence of apoptosis was investigated. Increased numbers of T cells expressing the activated phenotype CD25⁺, CD44^hi and CD62L^lo were detected 4 days after infection. Expression of CD25 (IL‐2Rα chain) on CD4⁺ and CD8⁺ T cells peaked at this time and returned to normal by day 7. In contrast, CD44^hi and CD62L^lo persisted, with the maximum proportion occurring at 7 days after infection. This was accompanied by a burst of in vivo proliferation of CD4⁺ and CD8⁺ T cells occurring between day 5 and 7. Apoptosis, which is presumably needed to control this expansion of T cells, also peaked at 7 days after infection. Apoptosis occurred preferentially amongst T cells which had proliferated. Most but not all proliferating T cells had down‐regulated their CD62L marker. While most apoptotic T cells were CD62L^lo, again not all had down‐regulated this marker. Hence, CD25 expression peaked early, but expression of other activation markers, in vivo proliferation and apoptosis coincided after Listeria infection. T cells that had proliferated were over‐represented in the apoptotic population.