tetano
Editor, Senior Moderator
Int Immunol. 2019 Oct 20. pii: dxz070. doi: 10.1093/intimm/dxz070. [Epub ahead of print] [h=1]ZBP1 governs the inflammasome-independent IL-1α and neutrophil inflammation that play a dual role in anti-influenza virus immunity.[/h]
Momota M[SUP]1,[/SUP][SUP]2,[/SUP][SUP]3[/SUP], Lelliott P[SUP]4[/SUP], Kubo A[SUP]1[/SUP], Kusakabe T[SUP]1,[/SUP][SUP]2,[/SUP][SUP]3[/SUP], Kobiyama K[SUP]1,[/SUP][SUP]5,[/SUP][SUP]6[/SUP], Kuroda E[SUP]1,[/SUP][SUP]3[/SUP], Imai Y[SUP]7[/SUP], Akira S[SUP]8[/SUP], Coban C[SUP]4,[/SUP][SUP]9,[/SUP][SUP]6[/SUP], Ishii KJ[SUP]1,[/SUP][SUP]2,[/SUP][SUP]3,[/SUP][SUP]5,[/SUP][SUP]6[/SUP].
[h=3]Author information[/h] 1 Laboratory of Adjuvant Innovation, Center for Vaccine and Adjuvant Research Center (CVAR), National Institutes of Biomedical Innovation, Health and Nutrition (NIBIOHN), Osaka, Japan. 2 Laboratory of Mockup Vaccine, Center for Vaccine and Adjuvant Research Center (CVAR), National Institutes of Biomedical Innovation, Health and Nutrition (NIBIOHN), Osaka, Japan. 3 Laboratory of Vaccine Science, World Premier International Immunology Frontier Research Center, Osaka University, Osaka, Japan. 4 Malaria immunology, World Premier International Immunology Frontier Research Center, Osaka University, Osaka, Japan. 5 Division of Vaccine Science, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan. 6 International Research and Development Center for Mucosal Vaccines, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan. 7 Laboratory of Regulation of Intractable Infectious Diseases, Center for Vaccine and Adjuvant Research Center (CVAR), National Institutes of Biomedical Innovation, Health and Nutrition (NIBIOHN), Osaka, Japan. 8 Host Defense, World Premier International Immunology Frontier Research Center, Osaka University, Osaka, Japan. 9 Division of Malaria Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
[h=3]Abstract[/h] Influenza A virus (IAV) triggers the infected lung to produce IL-1 and recruit neutrophil. Unlike IL-1β, however, little is known about IL-1α in terms of its mechanism of induction, action and physiological relevance to the host immunity against IAV infection. In particular, whether Z-DNA binding protein 1 (ZBP1), a key molecule for IAV-induced cell death, is involved in the IL-1α induction, neutrophil infiltration, and the physiological outcome have not been elucidated. Here we show in murine model that the IAV-induced IL-1α is mediated solely by ZBP1, in an NLRP3-inflammasome-independent manner, and is required for the optimal IL-1β production followed by the formation of neutrophil extracellular traps. During IAV infection, ZBP1 displays a dual role in anti-IAV immune responses mediated by neutrophil, resulting in either protective or pathological outcome in vivo. Thus, ZBP1-mediated IL-1α production is the key initial step of IAV-infected NETs, owing the duality of the consequent lung inflammation.
? The Author(s) 2019. Published by Oxford University Press on behalf of The Japanese Society for Immunology.
[h=4]KEYWORDS:[/h] IL-1; ZBP1; influenza virus; innate immunity; neutrophil
PMID: 31630209 DOI: 10.1093/intimm/dxz070
Momota M[SUP]1,[/SUP][SUP]2,[/SUP][SUP]3[/SUP], Lelliott P[SUP]4[/SUP], Kubo A[SUP]1[/SUP], Kusakabe T[SUP]1,[/SUP][SUP]2,[/SUP][SUP]3[/SUP], Kobiyama K[SUP]1,[/SUP][SUP]5,[/SUP][SUP]6[/SUP], Kuroda E[SUP]1,[/SUP][SUP]3[/SUP], Imai Y[SUP]7[/SUP], Akira S[SUP]8[/SUP], Coban C[SUP]4,[/SUP][SUP]9,[/SUP][SUP]6[/SUP], Ishii KJ[SUP]1,[/SUP][SUP]2,[/SUP][SUP]3,[/SUP][SUP]5,[/SUP][SUP]6[/SUP].
[h=3]Author information[/h] 1 Laboratory of Adjuvant Innovation, Center for Vaccine and Adjuvant Research Center (CVAR), National Institutes of Biomedical Innovation, Health and Nutrition (NIBIOHN), Osaka, Japan. 2 Laboratory of Mockup Vaccine, Center for Vaccine and Adjuvant Research Center (CVAR), National Institutes of Biomedical Innovation, Health and Nutrition (NIBIOHN), Osaka, Japan. 3 Laboratory of Vaccine Science, World Premier International Immunology Frontier Research Center, Osaka University, Osaka, Japan. 4 Malaria immunology, World Premier International Immunology Frontier Research Center, Osaka University, Osaka, Japan. 5 Division of Vaccine Science, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan. 6 International Research and Development Center for Mucosal Vaccines, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan. 7 Laboratory of Regulation of Intractable Infectious Diseases, Center for Vaccine and Adjuvant Research Center (CVAR), National Institutes of Biomedical Innovation, Health and Nutrition (NIBIOHN), Osaka, Japan. 8 Host Defense, World Premier International Immunology Frontier Research Center, Osaka University, Osaka, Japan. 9 Division of Malaria Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
[h=3]Abstract[/h] Influenza A virus (IAV) triggers the infected lung to produce IL-1 and recruit neutrophil. Unlike IL-1β, however, little is known about IL-1α in terms of its mechanism of induction, action and physiological relevance to the host immunity against IAV infection. In particular, whether Z-DNA binding protein 1 (ZBP1), a key molecule for IAV-induced cell death, is involved in the IL-1α induction, neutrophil infiltration, and the physiological outcome have not been elucidated. Here we show in murine model that the IAV-induced IL-1α is mediated solely by ZBP1, in an NLRP3-inflammasome-independent manner, and is required for the optimal IL-1β production followed by the formation of neutrophil extracellular traps. During IAV infection, ZBP1 displays a dual role in anti-IAV immune responses mediated by neutrophil, resulting in either protective or pathological outcome in vivo. Thus, ZBP1-mediated IL-1α production is the key initial step of IAV-infected NETs, owing the duality of the consequent lung inflammation.
? The Author(s) 2019. Published by Oxford University Press on behalf of The Japanese Society for Immunology.
[h=4]KEYWORDS:[/h] IL-1; ZBP1; influenza virus; innate immunity; neutrophil
PMID: 31630209 DOI: 10.1093/intimm/dxz070