Siglec Receptors Modulate Dendritic Cell Activation and Antigen Presentation to T Cells in Cancer.
antigen
antigen processing
glyco-immune checkpoint
sialic acid
tumor immunology
Journal
Frontiers in cell and developmental biology
ISSN: 2296-634X
Titre abrégé: Front Cell Dev Biol
Pays: Switzerland
ID NLM: 101630250
Informations de publication
Date de publication:
2022
2022
Historique:
received:
04
12
2021
accepted:
21
01
2022
entrez:
21
3
2022
pubmed:
22
3
2022
medline:
22
3
2022
Statut:
epublish
Résumé
Interactions between sialylated glycans and sialic acid-binding immunoglobulin-like lectin (Siglec) receptors have been recently described as potential new immune checkpoint that can be targeted to improve anticancer immunity. Myeloid cells have been reported to express a wide range of different Siglecs; however, their expression and functions on cancer-associated dendritic cells (DCs) were not fully characterized. We found that classical conventional DCs (cDCs) from cancer patient samples have a high expression of several inhibitory Siglecs including Siglec-7, Siglec-9, and Siglec-10. In subcutaneous murine tumor models, we also found an upregulation of the inhibitory Siglec-E receptor on cancer-associated cDCs. DC lines and bone marrow-derived DCs (BMDCs) with expression of these inhibitory Siglecs showed impaired maturation states on transcriptome and protein level. Furthermore, ablation of these inhibitory Siglecs from DCs enhanced their capability to prime antigen-specific T cells and induce proliferation. Our work provides a deeper understanding of the influence of inhibitory Siglecs on DCs and reveals a potential new target to improve cancer immunotherapy.
Identifiants
pubmed: 35309936
doi: 10.3389/fcell.2022.828916
pii: 828916
pmc: PMC8927547
doi:
Types de publication
Journal Article
Langues
eng
Pagination
828916Informations de copyright
Copyright © 2022 Wang, Manni, Bärenwaldt, Wieboldt, Kirchhammer, Ivanek, Stanczak, Zippelius, König, Rodrigues Manutano and Läubli.
Déclaration de conflit d'intérêts
HL received travel grants and consultant fees from Bristol-Myers Squibb (BMS) and Merck, Sharp and Dohme (MSD). HL received research support from BMS, GlycoEra, Novartis and Palleon Pharmaceuticals. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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