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

Thomas C. Wirth, Matthew D. Martin, Gabriel Starbeck-Miller, John T. Harty, Vladimir P. Badovinac

Research output: Contribution to journalArticlepeer-review

22 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)1321-1333
Number of pages13
JournalEuropean Journal of Immunology
Volume41
Issue number5
DOIs
StatePublished - May 2011
Externally publishedYes

Keywords

  • Inflammation
  • Memory
  • Secondary responses

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