Inflammasome recognition of influenza virus is essential for adaptive immune responses

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Influenza virus infection is recognized by the innate immune system through Toll like receptor (TLR) 7 and retinoic acid inducible gene I. These two recognition pathways lead to the activation of type I interferons and resistance to infection. In addition, TLR signals are required for the CD4 T cell and IgG2a, but not cytotoxic T lymphocyte, responses to influenza virus infection. In contrast, the role of NOD-like receptors (NLRs) in viral recognition and induction of adaptive immunity to influenza virus is unknown. We demonstrate that respiratory infection with influenza virus results in the activation of NLR inflammasomes in the lung. Although NLRP3 was required for inflammasome activation in certain cell types, CD4 and CD8 T cell responses, as well as mucosal IgA secretion and systemic IgG responses, required ASC and caspase-1 but not NLRP3. Consequently, ASC, caspase-1, and IL-1R, but not NLRP3, were required for protective immunity against flu challenge. Furthermore, we show that caspase-1 inflammasome activation in the hematopoietic, but not stromal, compartment was required to induce protective antiviral immunity. These results demonstrate that in addition to the TLR pathways, ASC inflammasomes play a central role in adaptive immunity to influenza virus.
Publisher
ROCKEFELLER UNIV PRESS
Issue Date
2009-01
Language
English
Article Type
Article
Keywords

CASPASE-1 ACTIVATION; NALP3 INFLAMMASOME; HUMAN MACROPHAGES; STRANDED-RNA; DYING CELLS; T-CELLS; A-VIRUS; INFECTION; INTERLEUKIN-1-BETA; CRYOPYRIN/NALP3

Citation

JOURNAL OF EXPERIMENTAL MEDICINE, v.206, no.1, pp.79 - 87

ISSN
0022-1007
DOI
10.1084/jem.20081667
URI
http://hdl.handle.net/10203/96624
Appears in Collection
MSE-Journal Papers(저널논문)
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