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Ishikawa, E., Ishikawa, T., Morita, Y.S., Toyonaga, K., Yamada, H., Takeuchi, O., Kinoshita, T., Akira, S., Yoshikai, Y. and Yamasaki, S. (2009) Direct Recognition of the Mycobacterial Glycolipid, Trehalose Dimycolate, by C-Type Lectin Mincle. Journal of Experimental Medicine, 206, 2879-2888.
https://doi.org/10.1084/jem.20091750

has been cited by the following article:

• 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.