tetano
Editor, Senior Moderator
Immunity. 2018 Aug 14. pii: S1074-7613(18)30331-5. doi: 10.1016/j.immuni.2018.07.011. [Epub ahead of print]
[h=1]Lung γδ T Cells Mediate Protective Responses during Neonatal Influenza Infection that Are Associated with Type 2 Immunity.[/h] Guo XJ[SUP]1[/SUP], Dash P[SUP]2[/SUP], Crawford JC[SUP]2[/SUP], Allen EK[SUP]2[/SUP], Zamora AE[SUP]2[/SUP], Boyd DF[SUP]2[/SUP], Duan S[SUP]2[/SUP], Bajracharya R[SUP]2[/SUP], Awad WA[SUP]2[/SUP], Apiwattanakul N[SUP]3[/SUP], Vogel P[SUP]4[/SUP], Kanneganti TD[SUP]2[/SUP], Thomas PG[SUP]5[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Compared to adults, infants suffer higher rates of hospitalization, severe clinical complications, and mortality due to influenza infection. We found that γδ T cells protected neonatal mice against mortality during influenza infection. γδ T cell deficiency did not alter viral clearance or interferon-γ production. Instead, neonatal influenza infection induced the accumulation of interleukin-17A (IL-17A)-producing γδ T cells, which was associated with IL-33 production by lung epithelial cells. Neonates lacking IL-17A-expressing γδ T cells or Il33 had higher mortality upon influenza infection. γδ T cells and IL-33 promoted lung infiltration of group 2 innate lymphoid cells and regulatory T cells, resulting in increased amphiregulin secretion and tissue repair. In influenza-infected children, IL-17A, IL-33, and amphiregulin expression were correlated, and increased IL-17A levels in nasal aspirates were associated with better clinical outcomes. Our results indicate that γδ T cells are required in influenza-infected neonates to initiate protective immunity and mediate lung homeostasis.
[h=4]KEYWORDS:[/h] IL-17A; IL-33; amphiregulin; children; neonatal influenza infection; type 2 immunity; γδ T cells
PMID: 30170813 DOI: 10.1016/j.immuni.2018.07.011
[h=1]Lung γδ T Cells Mediate Protective Responses during Neonatal Influenza Infection that Are Associated with Type 2 Immunity.[/h] Guo XJ[SUP]1[/SUP], Dash P[SUP]2[/SUP], Crawford JC[SUP]2[/SUP], Allen EK[SUP]2[/SUP], Zamora AE[SUP]2[/SUP], Boyd DF[SUP]2[/SUP], Duan S[SUP]2[/SUP], Bajracharya R[SUP]2[/SUP], Awad WA[SUP]2[/SUP], Apiwattanakul N[SUP]3[/SUP], Vogel P[SUP]4[/SUP], Kanneganti TD[SUP]2[/SUP], Thomas PG[SUP]5[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Compared to adults, infants suffer higher rates of hospitalization, severe clinical complications, and mortality due to influenza infection. We found that γδ T cells protected neonatal mice against mortality during influenza infection. γδ T cell deficiency did not alter viral clearance or interferon-γ production. Instead, neonatal influenza infection induced the accumulation of interleukin-17A (IL-17A)-producing γδ T cells, which was associated with IL-33 production by lung epithelial cells. Neonates lacking IL-17A-expressing γδ T cells or Il33 had higher mortality upon influenza infection. γδ T cells and IL-33 promoted lung infiltration of group 2 innate lymphoid cells and regulatory T cells, resulting in increased amphiregulin secretion and tissue repair. In influenza-infected children, IL-17A, IL-33, and amphiregulin expression were correlated, and increased IL-17A levels in nasal aspirates were associated with better clinical outcomes. Our results indicate that γδ T cells are required in influenza-infected neonates to initiate protective immunity and mediate lung homeostasis.
[h=4]KEYWORDS:[/h] IL-17A; IL-33; amphiregulin; children; neonatal influenza infection; type 2 immunity; γδ T cells
PMID: 30170813 DOI: 10.1016/j.immuni.2018.07.011