tetano
Editor, Senior Moderator
Am J Pathol. 2018 Feb 16. pii: S0002-9440(17)30887-8. doi: 10.1016/j.ajpath.2018.02.004. [Epub ahead of print]
[h=1]The LIM-only protein FHL2 supports influenza A virus-induced lung inflammation by restricting the host adaptive immune response.[/h] Masemann D[SUP]1[/SUP], Dantas RL[SUP]1[/SUP], Sitnik S[SUP]1[/SUP], Schied T[SUP]1[/SUP], Nordhoff C[SUP]1[/SUP], Ludwig S[SUP]2[/SUP], Wixler V[SUP]3[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] FHL2 is a multifunctional adaptor protein with fine-tuning adjustment properties. It acts as a regulator of signaling cascades but also as a cofactor of transcription and controls several anti-inflammatory immune responses. Recently, we described FHL2 as a novel regulator of influenza A virus propagation. We have shown that in vitro FHL2 restricts viral replication by accelerating the IRF-3-dependent transcription of the Ifnb1 gene. In this work, we unraveled an ambiguous role of FHL2 during influenza A virus infection in vivo. Although FHL2 restrained viral replication during the first 24h of infection, it significantly delayed viral clearance afterwards. Comparison of lung immune status of WT and FHL2 knockout (FHL2[SUP]KO[/SUP]) mice during influenza virus infection did not acknowledge significant differences in the innate host immune response but revealed an improved migration of dendritic cells from infected lungs into draining lymph nodes as well as increased levels of activated CD8[SUP]+[/SUP] T lymphocytes accumulated in the lungs of FHL2[SUP]KO[/SUP] mice.
PMID: 29458009 DOI: 10.1016/j.ajpath.2018.02.004
[h=1]The LIM-only protein FHL2 supports influenza A virus-induced lung inflammation by restricting the host adaptive immune response.[/h] Masemann D[SUP]1[/SUP], Dantas RL[SUP]1[/SUP], Sitnik S[SUP]1[/SUP], Schied T[SUP]1[/SUP], Nordhoff C[SUP]1[/SUP], Ludwig S[SUP]2[/SUP], Wixler V[SUP]3[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] FHL2 is a multifunctional adaptor protein with fine-tuning adjustment properties. It acts as a regulator of signaling cascades but also as a cofactor of transcription and controls several anti-inflammatory immune responses. Recently, we described FHL2 as a novel regulator of influenza A virus propagation. We have shown that in vitro FHL2 restricts viral replication by accelerating the IRF-3-dependent transcription of the Ifnb1 gene. In this work, we unraveled an ambiguous role of FHL2 during influenza A virus infection in vivo. Although FHL2 restrained viral replication during the first 24h of infection, it significantly delayed viral clearance afterwards. Comparison of lung immune status of WT and FHL2 knockout (FHL2[SUP]KO[/SUP]) mice during influenza virus infection did not acknowledge significant differences in the innate host immune response but revealed an improved migration of dendritic cells from infected lungs into draining lymph nodes as well as increased levels of activated CD8[SUP]+[/SUP] T lymphocytes accumulated in the lungs of FHL2[SUP]KO[/SUP] mice.
PMID: 29458009 DOI: 10.1016/j.ajpath.2018.02.004