Evidence map›Paper›PMID 38448555›Full record

ArticleCellular & molecular immunology2024

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

Ronja Wieboldt, Michael Sandholzer, Emanuele Carlini, Chia-Wei Lin, Anastasiya Börsch, Andreas Zingg, Didier Lardinois, Petra Herzig, Leyla Don, Alfred Zippelius and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Cellular & molecular immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
7.2field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 31 citations in OpenAlex.

  1. Sialic acidOncoimmunology · 2026
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  6. Pharmaceuticals (Basel, Switzerland) · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 1 country.

Ronja WieboldtLaboratory for Cancer Immunotherapy, Department of Biomedicine, University Hospital and University of Basel, Basel, Switzerland.
Michael SandholzerLaboratory for Cancer Immunotherapy, Department of Biomedicine, University Hospital and University of Basel, Basel, Switzerland.
Emanuele CarliniLaboratory for Cancer Immunotherapy, Department of Biomedicine, University Hospital and University of Basel, Basel, Switzerland.
Chia-Wei LinFunctional Genomics Center Zurich, ETH Zurich, Zurich, Switzerland.ORCID 0000-0003-4777-2916
Anastasiya BörschBioinformatics Core Facility, Department of Biomedicine, University of Basel and Swiss Institute of Bioinformatics, Basel, Switzerland.
Andreas ZinggLaboratory for Cancer Immunotherapy, Department of Biomedicine, University Hospital and University of Basel, Basel, Switzerland.
Didier LardinoisDepartment of Thoracic Surgery, University Hospital Basel, Basel, Switzerland.
Petra HerzigLaboratory of Cancer Immunology, Department of Biomedicine, University Hospital and University of Basel, Basel, Switzerland.
Leyla DonLaboratory of Cancer Immunology, Department of Biomedicine, University Hospital and University of Basel, Basel, Switzerland.
Alfred ZippeliusLaboratory of Cancer Immunology, Department of Biomedicine, University Hospital and University of Basel, Basel, Switzerland.
Heinz Läubli *Laboratory for Cancer Immunotherapy, Department of Biomedicine, University Hospital and University of Basel, Basel, Switzerland. heinz.laeubli@unibas.ch.ORCID 0000-0002-8910-5620
Natalia Rodrigues Mantuano *Laboratory for Cancer Immunotherapy, Department of Biomedicine, University Hospital and University of Basel, Basel, Switzerland. natalia.rodriguesmantuano@unibas.ch.
University of Basel · CHUniversity Hospital of Basel · CHETH Zurich · CHSIB Swiss Institute of Bioinformatics · CH

Funding

Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (Swiss National Science Foundation) 310030-184720
6 · The paper itself

Abstract

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.

Indexed as

Chemokine CCL2Mice, Inbred C57BLMyeloid-Derived Suppressor CellsPolysaccharidesSialic Acid Binding Immunoglobulin-like LectinsAnimalsCell Line, TumorHumansLung NeoplasmsMiceMice, KnockoutN-Acetylneuraminic AcidT-LymphocytesChemokine CCL2N-Acetylneuraminic AcidPolysaccharidesSialic Acid Binding Immunoglobulin-like Lectinsmyeloid derived suppressor cellsSialic acid-binding immunoglobulin-like lectinsialoglycanstumor microenvironment

Identifiers

PMID38448555
PMCPMC11061307
OpenAlexW4392508479

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.