Engagement of sialylated glycans with Siglec receptors on suppressive myeloid cells inhibits anticancer immunity via CCL2.

Sialic acid-binding immunoglobulin-like lectin myeloid derived suppressor cells sialoglycans tumor microenvironment

Journal

Cellular & molecular immunology
ISSN: 2042-0226
Titre abrégé: Cell Mol Immunol
Pays: China
ID NLM: 101242872

Informations de publication

Date de publication:
06 Mar 2024
Historique:
received: 14 08 2023
accepted: 30 01 2024
medline: 7 3 2024
pubmed: 7 3 2024
entrez: 6 3 2024
Statut: aheadofprint

Résumé

The overexpression of sialic acids on glycans, called hypersialylation, is a common alteration found in cancer cells. Sialylated glycans can enhance immune evasion by interacting with sialic acid-binding immunoglobulin-like lectin (Siglec) receptors on tumor-infiltrating immune cells. Here, we investigated the effect of sialylated glycans and their interaction with Siglec receptors on myeloid-derived suppressor cells (MDSCs). We found that MDSCs derived from the blood of lung cancer patients and tumor-bearing mice strongly express inhibitory Siglec receptors and are highly sialylated. In murine cancer models of emergency myelopoiesis, Siglec-E knockout in myeloid cells resulted in prolonged survival and increased tumor infiltration of activated T cells. Targeting suppressive myeloid cells by blocking Siglec receptors or desialylation strongly reduced their suppressive potential. We further identified CCL2 as a mediator involved in T-cell suppression upon interaction between sialoglycans and Siglec receptors on MDSCs. Our results demonstrated that sialylated glycans inhibit anticancer immunity by modulating CCL2 expression.

Identifiants

pubmed: 38448555
doi: 10.1038/s41423-024-01142-0
pii: 10.1038/s41423-024-01142-0
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (Swiss National Science Foundation)
ID : 310030-184720

Informations de copyright

© 2024. The Author(s).

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Auteurs

Ronja Wieboldt (R)

Laboratory for Cancer Immunotherapy, Department of Biomedicine, University Hospital and University of Basel, Basel, Switzerland.

Michael Sandholzer (M)

Laboratory for Cancer Immunotherapy, Department of Biomedicine, University Hospital and University of Basel, Basel, Switzerland.

Emanuele Carlini (E)

Laboratory for Cancer Immunotherapy, Department of Biomedicine, University Hospital and University of Basel, Basel, Switzerland.

Chia-Wei Lin (CW)

Functional Genomics Center Zurich, ETH Zurich, Zurich, Switzerland.

Anastasiya Börsch (A)

Bioinformatics Core Facility, Department of Biomedicine, University of Basel and Swiss Institute of Bioinformatics, Basel, Switzerland.

Andreas Zingg (A)

Laboratory for Cancer Immunotherapy, Department of Biomedicine, University Hospital and University of Basel, Basel, Switzerland.

Didier Lardinois (D)

Department of Thoracic Surgery, University Hospital Basel, Basel, Switzerland.

Petra Herzig (P)

Laboratory of Cancer Immunology, Department of Biomedicine, University Hospital and University of Basel, Basel, Switzerland.

Leyla Don (L)

Laboratory of Cancer Immunology, Department of Biomedicine, University Hospital and University of Basel, Basel, Switzerland.

Alfred Zippelius (A)

Laboratory of Cancer Immunology, Department of Biomedicine, University Hospital and University of Basel, Basel, Switzerland.
Division of Oncology, University Hospital Basel, Basel, Switzerland.

Heinz Läubli (H)

Laboratory for Cancer Immunotherapy, Department of Biomedicine, University Hospital and University of Basel, Basel, Switzerland. heinz.laeubli@unibas.ch.
Division of Oncology, University Hospital Basel, Basel, Switzerland. heinz.laeubli@unibas.ch.

Natalia Rodrigues Mantuano (NR)

Laboratory for Cancer Immunotherapy, Department of Biomedicine, University Hospital and University of Basel, Basel, Switzerland. natalia.rodriguesmantuano@unibas.ch.

Classifications MeSH