Evidence map›Paper›PMID 42842659›Full record

ArticleScience advances2026

Kupffer cells are key mediators of antigen-specific immune tolerance by peptide-coupled red blood cells.

Vasileia Kalaitzaki, Pietro Oldrati, Filipa M Ferreira, Antonios Katsoulas, Ahmed Ali, Livio Baselgia, Yun Liu, Jincheng Fang, Roman Sankowski, Mai Matsushita and 6 more

Abstract read
In one paragraph

Article in Science advances, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

16 authors.

Vasileia KalaitzakiInstitute of Laboratory Animal Science, University of Zurich, Schlieren, Switzerland.ORCID 0000-0002-4158-2321
Pietro OldratiCellerys AG, Wagistrasse 21, Schlieren, Switzerland.ORCID 0000-0001-5551-4306
Filipa M FerreiraInstitute of Laboratory Animal Science, University of Zurich, Schlieren, Switzerland.ORCID 0000-0003-2465-3121
Antonios KatsoulasInstitute of Laboratory Animal Science, University of Zurich, Schlieren, Switzerland.ORCID 0000-0001-8138-7646
Ahmed AliInstitute of Laboratory Animal Science, University of Zurich, Schlieren, Switzerland.ORCID 0009-0009-0335-1491
Livio BaselgiaDepartment of Internal Medicine, University Hospital and University of Zurich, Zurich, Switzerland.ORCID 0000-0003-2583-8195
Yun LiuInstitute for Neuropathology, University Hospital Freiburg, Freiburg, Germany.
Jincheng FangInstitute for Neuropathology, University Hospital Freiburg, Freiburg, Germany.ORCID 0000-0002-6736-7064
Roman SankowskiInstitute for Neuropathology, University Hospital Freiburg, Freiburg, Germany.ORCID 0000-0001-9215-8021
Mai MatsushitaInstitute of Laboratory Animal Science, University of Zurich, Schlieren, Switzerland.ORCID 0000-0001-5693-461X
Florence VallelianDepartment of Internal Medicine, University Hospital and University of Zurich, Zurich, Switzerland.
Alexandre P A TheocharidesDepartment of Medical Oncology and Hematology, University of Zurich and University Hospital, Zurich, Switzerland.ORCID 0000-0002-1535-8692
Cyrill GéraudSection of Molecular and Clinical Dermatology, Department of Dermatology, Venereology and Allergology and European Center for Angioscience, University Medical Center and Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.ORCID 0000-0001-9432-6869
Roland MartinCellerys AG, Wagistrasse 21, Schlieren, Switzerland.ORCID 0000-0002-0982-1329
Andreas LutterottiCellerys AG, Wagistrasse 21, Schlieren, Switzerland.ORCID 0000-0003-1301-2863
Thorsten BuchInstitute of Laboratory Animal Science, University of Zurich, Schlieren, Switzerland.ORCID 0000-0002-2236-9074

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Induction of antigen-specific immune tolerance is the most precise method for reverting an autoreactive immune response in diseases such as multiple sclerosis (MS). Coupling red blood cells (RBCs) with a cocktail of MS immunodominant peptides is a promising approach to induce antigen-specific immune tolerance in patients. Here, we show that RBCs coupled with disease-inducing antigen efficiently prevent the development of experimental autoimmune encephalomyelitis, when administered prophylactically, and ameliorate disease symptoms when given therapeutically. The tolerogenic activity of peptide-coupled RBCs (pcRBC) was antigen specific and dependent on both cell and peptide dose. Kupffer cells (KC) were the primary phagocytes of pcRBC, and their uptake of pcRBC did not require complement component 3, SIRPα, and Stabilin 1 and 2. KC were indispensable for the induction of tolerance, which was accompanied by programmed death-ligand 1 up-regulation and a tolerogenic transcriptional shift. Our findings establish KC as central mediators of pcRBC-induced immune tolerance and provide mechanistic insight for the use of this therapeutic strategy in autoimmune disease.

Indexed as

AntigensErythrocytesImmune ToleranceKupffer CellsPeptidesAnimalsEncephalomyelitis, Autoimmune, ExperimentalFemaleHumansMiceAntigensPeptides

Identifiers

PMID42842659
PMCPMC13644765

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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.