2021年7月12日
Role of Dectin-2 in the phagocytosis of Cryptococcus neoformans by dendritic cells.
Infection and immunity
- 巻
- 89
- 号
- 10
- 開始ページ
- IAI0033021
- 終了ページ
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1128/IAI.00330-21
The cell walls and capsules of Cryptococcus neoformans, a yeast-type fungal pathogen, are rich in polysaccharides. Dectin-2 is a C-type lectin receptor (CLR) that recognizes high-mannose polysaccharides. Previously, we demonstrated that Dectin-2 is involved in cytokine production by bone marrow-derived dendritic cells (BM-DCs) in response to stimulation with C. neoformans. In the present study, we analyzed the role of Dectin-2 in the phagocytosis of C. neoformans by BM-DCs. The engulfment of this fungus by BM-DCs was significantly decreased in mice lacking Dectin-2 (Dectin-2KO) or caspase recruitment domain-containing protein 9 (CARD9KO), a common adapter molecule that delivers signals triggered by CLRs, compared to wild-type (WT) mice. Phagocytosis was likewise inhibited, to a similar degree, by the inhibition of Syk, a signaling molecule involved in CLR-triggered activation. A PI3K inhibitor, in contrast, completely abrogated the phagocytosis of C. neoformans. Actin polymerization, i.e., conformational changes in cytoskeletons detected at sites of contact with C. neoformans, was also decreased in BM-DCs of Dectin-2KO and CARD9KO mice. Finally, the engulfment of C. neoformans by macrophages was significantly decreased in the lungs of Dectin-2KO mice compared to WT mice. These results suggest that Dectin-2 may play an important role in the actin polymerization and phagocytosis of C. neoformans by DCs, possibly through signaling via CARD9 and a signaling pathway mediated by Syk and PI3K.
- リンク情報
-
- DOI
- https://doi.org/10.1128/IAI.00330-21
- PubMed
- https://www.ncbi.nlm.nih.gov/pubmed/34251289
- PubMed Central
- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8445189
- Scopus
- https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85115952506&origin=inward
- Scopus Citedby
- https://www.scopus.com/inward/citedby.uri?partnerID=HzOxMe3b&scp=85115952506&origin=inward
- ID情報
-
- DOI : 10.1128/IAI.00330-21
- ISSN : 0019-9567
- eISSN : 1098-5522
- PubMed ID : 34251289
- PubMed Central 記事ID : PMC8445189
- SCOPUS ID : 85115952506