Inflammasome recognition of influenza virus is essential for adaptive immune responses

Takeshi Ichinohe et al. J. Exp. Med. 206: 79 - 87 ( 2009 )

Student: Chih-Yuan Kuo (郭芝源）                             Time: 13:10~14:00 May. 27, 2009

Commentator: Dr. Chiou-Feng Lin (林秋烽老師）    Place: Room 601

Abstract:

Previous studies indicated that influenza virus infection is recognized by the innate immune system through Toll-like receptor (TLR) 7 and retinoic acid inducible gene I. Signaling through both RIG-I and TLR7 results in the production of type I IFNs, which limit viral replication and increase resistance to infection. IL-1 also plays a crucial role in protection against influenza¹. The NOD-like receptors (NLR) are a family of intracellular sensors of microbial motifs and danger signals. A number of NLR family members can form multiprotein complexes, called inflammasomes.Inflammasomes are molecular platforms to allow activation of caspase-1². Caspase-1 is an essential regulator of inflammatory response through its capacity to process and activate proIL-1β, and proIL-18³. Although the proinflammatory role of inflammasomes is well known, the role of inflammasomes in the recognition of viral infection in vivo and generation of protective adaptive immunity is unknown. In this paper, NLRP3 inflammasome is activated in the lung after respiratory influenza infection. Furthermore, the authors used mice defective in inflammasome components NLRP3, ASC, or Caspase-1 and BM chimeric mice to detect the production of IL-1β, and to evaluate the effect of T cell and B cell. The results indicate that inflammasomes play an important role in protection against influenza infection. These data have significant implications in the design of prophylactic vaccines and management of influenza infection in general.

References:

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2.     Virginie Pe´ trilli, et al. The inflammasome: a danger sensing complex triggering innate immunity. Current Opinion in Immunology , 2007, 19:615–622

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