Secondary CD8+ T-cell responses are controlled by systemic inflammation.
Eur J Immunol
; 41(5): 1321-33, 2011 May.
Article
em En
| MEDLINE
| ID: mdl-21425157
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.
Texto completo:
1
Bases de dados:
MEDLINE
Assunto principal:
Ativação Linfocitária
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Imunização Secundária
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Linfócitos T CD8-Positivos
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Memória Imunológica
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Inflamação
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Listeriose
Limite:
Animals
Idioma:
En
Revista:
Eur J Immunol
Ano de publicação:
2011
Tipo de documento:
Article
País de afiliação:
Estados Unidos