Secondary CD8+ T‐cell responses are controlled by systemic inflammation

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Abstract
Repeated infections and experimental prime‐boost regimens frequently result in the generation of secondary (2°) CD8+ T‐cell responses. In contrast to primary (1°) CD8+ T cells, the parameters that influence the abundance and phenotype of 2° effector and memory CD8+ T‐cell populations are largely unknown. Here, we analyze the impact of different booster infections, Ag curtailment, and systemic inflammation on the quality and quantity of secondary CD8+ T‐cell responses. We show that similar to 1° CD8+ T‐cell responses, the phenotype of 2° effector and memory CD8+ T‐cell populations is critically dependent on the nature of the infectious pathogen and the inflammatory milieu early after infection. In addition, systemic inflammation increases the number of 2° effector and memory CD8+ T cells after booster infections and immunizations. Therefore, our data reveal new means to boost the number of 2° effector and memory CD8+ T cells in prime‐boost regimens and show a surprisingly high degree of plasticity in 2° memory CD8+ T‐cell phenotype that is controlled by systemic inflammation.