Evidence map›Paper›PMID 40076664›Full record

ArticleInternational journal of molecular sciences2025

CXCR4 Inhibition Enhances the Efficacy of CD19 Monoclonal Antibody-Mediated Extermination of B-Cell Lymphoma.

Nupur Khunti, Manish Kumar, Moumita Datta, Jean de Dieu Harelimana, Mirja Harms, Dan Albers, Frank Kirchhoff, Jan Münch, Steffen Stenger, Christian Buske and 1 more

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. IGLV3-21HemaSphere · 2026
    Article
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

11 authors.

Nupur KhuntiInstitute of Experimental Cancer Research, Ulm University Medical Center, 89081 Ulm, Germany.
Manish KumarInstitute of Experimental Cancer Research, Ulm University Medical Center, 89081 Ulm, Germany.
Moumita DattaInstitute of Immunology, Ulm University Medical Center, 89081 Ulm, Germany.ORCID 0009-0004-6524-4804
Jean de Dieu HarelimanaInstitute of Microbiology and Hygiene, Ulm University Medical Center, 89081 Ulm, Germany.
Mirja HarmsInstitute of Molecular Virology, Ulm University Medical Center, 89081 Ulm, Germany.ORCID 0000-0002-5460-5166
Dan AlbersInstitute of Molecular Virology, Ulm University Medical Center, 89081 Ulm, Germany.
Frank KirchhoffInstitute of Molecular Virology, Ulm University Medical Center, 89081 Ulm, Germany.ORCID 0000-0002-7052-2360
Jan MünchInstitute of Molecular Virology, Ulm University Medical Center, 89081 Ulm, Germany.ORCID 0000-0001-7316-7141
Steffen StengerInstitute of Microbiology and Hygiene, Ulm University Medical Center, 89081 Ulm, Germany.
Christian BuskeInstitute of Experimental Cancer Research, Ulm University Medical Center, 89081 Ulm, Germany.
Palash Chandra MaityInstitute of Experimental Cancer Research, Ulm University Medical Center, 89081 Ulm, Germany.ORCID 0000-0003-3295-5859

Funding

Deutsche Forschungsgemeinschaft CRC1279 project B01Fritz Thyssen Stiftung 10.23.1.012MN
6 · The paper itself

Abstract

CD19 and CXCR4 are pivotal regulators of B-cell activation and migration, respectively. Specifically, CXCR4 signaling critically influences the dissemination of various malignant B cells through constitutive activation and aberrant expression. This study explores the interaction between CD19 and CXCR4 signaling in the context of B-cell lymphomas, particularly focusing on diffuse large B-cell lymphoma (DLBCL) and Waldenström Macroglobulinemia (WM). We assessed the roles of CD19 in survival and CXCL12-induced migration by using knockout (KO) cells of DLBCL and WM origin alongside evaluating the impact of CD19 monoclonal antibodies (mAbs) on antibody-dependent cell-mediated cytotoxicity (ADCC). Our results highlight that CD19 is important for survival and CXCL12-induced migration, and mAbs variably increase CXCL12-induced migration and enhance ADCC. Additionally, we demonstrate that the endogenous peptide inhibitor of the CXCR4 (EPI-X4) derivative JM#21 effectively inhibits CD19-mediated migration enhancement and promotes ADCC, thereby augmenting the therapeutic efficacy of CD19 mAb-based immunotherapy in lymphoma models. Our study underscores the potential of targeting both CD19 and CXCR4 to refine therapeutic strategies for treating B-cell malignancies, suggesting a synergistic approach could improve clinical outcomes in WM treatment.

Indexed as

Antibodies, MonoclonalAntigens, CD19Lymphoma, B-CellLymphoma, Large B-Cell, DiffuseReceptors, CXCR4AnimalsAntibody-Dependent Cell CytotoxicityCell Line, TumorCell MovementChemokine CXCL12HumansMiceWaldenstrom MacroglobulinemiaAntibodies, MonoclonalAntigens, CD19CD19 molecule, humanChemokine CXCL12CXCR4 protein, humanReceptors, CXCR4B-cell lymphomaCD19CXCR4monoclonal antibody (mAb)Waldenström Macroglobulinemia (WM)

Identifiers

PMID40076664
PMCPMC11899823

What OpenQuestion holds

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Registered trials

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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.