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Teng, O., Chen, S., Hsu, T., Sia, S.F., Cole, S., Valkenburg, S.A., Hsu, T., Zheng, J.T., Tu, W., Bruzzone, R., Peiris, J.S.M., Hsieh, S. and Yen, H. (2016) CLEC5A-Mediated Enhancement of the Inflammatory Response in Myeloid Cells Contributes to Influenza Virus Pathogenicity in Vivo. Journal of Virology, 91, e01813-e01816.
https://doi.org/10.1128/jvi.01813-16
has been cited by the following article:
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TITLE:
Involvement of Dectin-2 in the Innate Inflammatory Response Triggered by Influenza Virus Hemagglutinin
AUTHORS:
Hideki Yamamoto, Chikako Tomiyama, Sho Yamasaki, Shinobu Saijo, Yoichiro Iwakura, Kazuyoshi Kawakami
KEYWORDS:
C-Type Lectin Receptors, Influenza Virus, Innate Immunity, Type I Interferon
JOURNAL NAME:
Advances in Infectious Diseases,
Vol.13 No.3,
September
20,
2023
ABSTRACT: C-type lectin receptors (CLRs) are representative pattern recognition receptors that recognize microbial polysaccharides expressed on antigen-presenting cells. In the present study, we carried out further detailed analysis on the involvement of Dectin-2, a CLR that senses high mannose polysaccharide, in innate immune responses induced by influenza virus hemagglutinin (HA). Treatment of HA with periodate or PNGase F induced lower interleukin (IL)-12p40 secretion by conventional dendritic cells (DCs) compared with the untreated group. In contrast, treatment with O-glycosidase did not affect cytokine production. Green fluorescent protein expression in canonical Dectin-2-transducing cells was approximately 3% - 12% following HA stimulation, except with the A/H1N1pdm09 subtype HA. This expression was markedly reduced in cells possessing mutated amino acids in the carbohydrate recognition domain of Dectin-2, especially following stimulation with HA derived from the A/H3N2 subtype. Interferon (IFN)-α production from CD11c+Siglec-H+PDCA-1+ plasmacytoid DCs was significantly increased in Dectin-2 knockout mice compared with wild-type mice upon stimulation with HA except for the B/Yamagata lineage HA. These results suggested that Dectin-2 is involved in initiating inflammatory responses via mannose polysaccharide on HA. However, other mechanisms may function in the antiviral response, including the type I IFN axis.