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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Immunol
2018 ; 201
(2
): 573-582
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gab.com Text
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IL-36? Protects against Severe Influenza Infection by Promoting Lung Alveolar
Macrophage Survival and Limiting Viral Replication
#MMPMID29848754
Wein AN
; Dunbar PR
; McMaster SR
; Li ZT
; Denning TL
; Kohlmeier JE
J Immunol
2018[Jul]; 201
(2
): 573-582
PMID29848754
show ga
Although influenza virus infection remains a concerning disease for public
health, the roles of individual cytokines during the immune response to influenza
infection are not fully understood. We have identified IL-36? as a key mediator
of immune protection during both high- and low-pathogenesis influenza infection.
Il36g mRNA is upregulated in the lung following influenza infection, and mice
lacking IL-36? have greatly increased morbidity and mortality upon infection with
either H1N1 or H3N2 influenza. The increased severity of influenza infection in
IL-36?-knockout (KO) mice is associated with increased viral titers, higher
levels of proinflammatory cytokines early in infection, and more diffuse
pathologic conditions late in the disease course. Interestingly, the increased
severity of disease in IL-36?-KO mice correlates with a rapid loss of alveolar
macrophages following infection. We find that the alveolar macrophages from naive
IL-36?-KO mice have higher expression of M2-like surface markers compared with
wild-type (WT) mice and show increased apoptosis within 24 h of infection.
Finally, transfer of WT alveolar macrophages to IL-36?-KO mice restores
protection against lethal influenza challenge to levels observed in WT mice.
Together, these data identify a critical role for IL-36? in immunity against
influenza virus and demonstrate the importance of IL-36? signaling for alveolar
macrophage survival during infection.
|Adoptive Transfer
[MESH]
|Animals
[MESH]
|Cell Survival
[MESH]
|Cells, Cultured
[MESH]
|Humans
[MESH]
|Influenza A Virus, H1N1 Subtype/*physiology
[MESH]
|Influenza A Virus, H3N2 Subtype/*physiology
[MESH]