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Secondary CD8+ T-cell responses are controlled by systemic inflammation
Journal article   Open access   Peer reviewed

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

Thomas C Wirth, Matthew D Martin, Gabriel Starbeck-Miller, John T Harty and Vladimir P Badovinac
European journal of immunology, Vol.41(5), pp.1321-1333
05/2011
DOI: 10.1002/eji.201040730
PMCID: PMC3083480
PMID: 21425157
url
https://doi.org/10.1002/eji.201040730View
Published (Version of record) Open Access

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.
Memory Inflammation Secondary responses

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