Dissemin is shutting down on January 1st, 2025

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Wiley, European Journal of Immunology, 5(41), p. 1321-1333, 2011

DOI: 10.1002/eji.201040730

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

This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Data provided by SHERPA/RoMEO

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.