Journal
IMMUNOLOGY AND CELL BIOLOGY
Volume 94, Issue 5, Pages 439-446Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/icb.2015.115
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Funding
- National Health and Medical Research Council of Australia (NHMRC) [1026619, 1079924]
- NHMRC [1071916]
- National Health and Medical Research Council of Australia [1079924, 1071916] Funding Source: NHMRC
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Expression of the viral virulence protein PB1-F2 during infection has been linked to NLRP3 inflammasome complex activation in macrophages and induction of early inflammatory events enhancing immunopathology during influenza disease. We sought to determine whether PB1-F2-specific NLRP3 inflammasome activation influenced the magnitude and/or robustness of the CD8(+) T-cell responses specific for conserved viral antigens and subsequent virus elimination. Using murine heterosubtypic viral infection models, we showed that mice infected with virus unable to produce PB1-F2 protein showed no deficit in the overall magnitude and functional memory responses of CD8(+) T cells established during the effector phase compared with those infected with wild-type PB1-F2-expressing virus and were equally capable of mounting robust recall responses. These data indicate that while expression of PB1-F2 protein can induce inflammatory events, the capacity to generate memory CD8(+) T cells specific for immunodominant viral epitopes remains uncompromised.
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