tetano
Editor, Senior Moderator
Innate immune response to influenza virus.
Wu S, Metcalf JP, Wu W.
aDepartment of Emergency and Critical Care, the Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China bPulmonary and Critical Care Division, Department of Medicine, USA cDepartment of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.
Abstract
PURPOSE OF REVIEW: The recent pandemic of a novel H1N1 influenza virus has stressed the importance of effective approaches to prevent viral infection. The innate immune system is our first line of defense against invading viruses. This review aims to give a brief summary of recent findings on the response of the innate immune system to influenza virus.
RECENT FINDINGS: Three families of pattern recognition receptors, toll-like receptors (TLRs), retinoic acid-inducible gene 1 protein like helicases (RLRs) and nucleotide-binding domain and leucine-rich-repeat-containing proteins (NLRs), are involved in recognition of influenza virus and they cooperatively operate to respond to the virus in cell culture or mouse models. Influenza virus mainly induces two types of innate immune cytokine responses: a proinflammatory response and an antiviral response. Recently, the NLRP3 inflammasome has proved to be an essential component in the host defense against influenza infection. The mitochondrion, traditionally recognized for its key role in respiration, metabolism and apoptosis, is becoming recognized as an important organelle for regulation of innate immune responses to influenza virus.
SUMMARY: The NLRP3 inflammasome is an essential component in the host defense against influenza infection. Further investigations are required to elucidate whether NLRP3 is associated with the adaptive response and to identify the components of influenza virus that activate this important mediator. The role of mitochondria as a potential central platform of innate response is becoming appreciated.
PMID: 21330918 [PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/21330918
Wu S, Metcalf JP, Wu W.
aDepartment of Emergency and Critical Care, the Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China bPulmonary and Critical Care Division, Department of Medicine, USA cDepartment of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.
Abstract
PURPOSE OF REVIEW: The recent pandemic of a novel H1N1 influenza virus has stressed the importance of effective approaches to prevent viral infection. The innate immune system is our first line of defense against invading viruses. This review aims to give a brief summary of recent findings on the response of the innate immune system to influenza virus.
RECENT FINDINGS: Three families of pattern recognition receptors, toll-like receptors (TLRs), retinoic acid-inducible gene 1 protein like helicases (RLRs) and nucleotide-binding domain and leucine-rich-repeat-containing proteins (NLRs), are involved in recognition of influenza virus and they cooperatively operate to respond to the virus in cell culture or mouse models. Influenza virus mainly induces two types of innate immune cytokine responses: a proinflammatory response and an antiviral response. Recently, the NLRP3 inflammasome has proved to be an essential component in the host defense against influenza infection. The mitochondrion, traditionally recognized for its key role in respiration, metabolism and apoptosis, is becoming recognized as an important organelle for regulation of innate immune responses to influenza virus.
SUMMARY: The NLRP3 inflammasome is an essential component in the host defense against influenza infection. Further investigations are required to elucidate whether NLRP3 is associated with the adaptive response and to identify the components of influenza virus that activate this important mediator. The role of mitochondria as a potential central platform of innate response is becoming appreciated.
PMID: 21330918 [PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/21330918