TY - JOUR
T1 - Secondary CD8+ T-cell responses are controlled by systemic inflammation
AU - Wirth, Thomas C.
AU - Martin, Matthew D.
AU - Starbeck-Miller, Gabriel
AU - Harty, John T.
AU - Badovinac, Vladimir P.
PY - 2011/5
Y1 - 2011/5
N2 - 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.
AB - 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.
KW - Inflammation
KW - Memory
KW - Secondary responses
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U2 - 10.1002/eji.201040730
DO - 10.1002/eji.201040730
M3 - Article
C2 - 21425157
AN - SCOPUS:79955142273
SN - 0014-2980
VL - 41
SP - 1321
EP - 1333
JO - European Journal of Immunology
JF - European Journal of Immunology
IS - 5
ER -