Distinct autoreactive CD19– plasma cell subsets accumulate in lupus-prone mice

Dang Van Duc, Franziska Szelinski, Elodie Mohr, Tuan Anh Le, Jacob Ritter, Annika Wiedemann, Marta Ferreira-Gomes, Gabriela Maria Guerra, Pawel Durek, Frederik Heinrich, Hector Rincon-Arevalo, Ana-Luisa Stefanski, Eva Schrezenmeier, Hoang Van T., Hong-Nhung Dao, Soeren Ocvirk, Qingyu Cheng, Falk Hiepe, Christian Hipfl, Sebastian Hardt, Max Löhning, Liem Thanh Nguyen, Mir-Farzin Mashreghi, Simon Fillatreau, Thomas Dörner and Andreia C. Lino ()
Additional contact information
Dang Van Duc: a Leibniz Institute
Franziska Szelinski: a Leibniz Institute
Elodie Mohr: a Leibniz Institute
Tuan Anh Le: a Leibniz Institute
Jacob Ritter: a Leibniz Institute
Annika Wiedemann: a Leibniz Institute
Marta Ferreira-Gomes: a Leibniz Institute
Gabriela Maria Guerra: a Leibniz Institute
Pawel Durek: a Leibniz Institute
Frederik Heinrich: a Leibniz Institute
Hector Rincon-Arevalo: a Leibniz Institute
Ana-Luisa Stefanski: a Leibniz Institute
Eva Schrezenmeier: a Leibniz Institute
Hoang Van T.: Vinhomes Ocean Park
Hong-Nhung Dao: Vinhomes Ocean Park
Soeren Ocvirk: German Institute of Human Nutrition Potsdam-Rehbruecke
Qingyu Cheng: a Leibniz Institute
Falk Hiepe: a Leibniz Institute
Christian Hipfl: Charité Universitätsmedizin Berlin
Sebastian Hardt: Charité Universitätsmedizin Berlin
Max Löhning: a Leibniz Institute
Liem Thanh Nguyen: Vinhomes Ocean Park
Mir-Farzin Mashreghi: a Leibniz Institute
Simon Fillatreau: INSERM U1151-CNRS UMR 8253
Thomas Dörner: a Leibniz Institute
Andreia C. Lino: a Leibniz Institute

Nature Communications, 2025, vol. 16, issue 1, 1-20

Abstract: Abstract Plasma cells (PC) participate in the pathogenesis of systemic lupus erythematosus (SLE) through sustained autoantibody and inflammatory cytokine secretion. Current PC-depleting therapies risk eliminating protective long-lived PCs, highlighting the need to identify pathogenic subsets for selective targeting. Here, using single-cell RNA sequencing, B cell receptor repertoire analysis, and genetic models, we identify disease- and organ-specific PCs in lupus-prone mice. We find a substantial expansion of autoreactive CD19– PCs, particularly class-switched CXCR3⁺ and phosphatidylcholine-specific B-1–derived subsets, which exhibit unique gene expression profiles. We show that CD19– PCs originate from CD19+ PCs in a unidirectional manner. Peripheral blood from SLE patients shows elevated frequencies of CD19– PCs, implicating these cells in sustaining pathogenic activity. Our findings highlight the emergence of autoreactive CD19– PCs as a critical feature of lupus pathogenesis in mice and underscore the need for therapeutic approaches that extend beyond CD19-targeting to improve treatment strategies in SLE.

Date: 2025
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/s41467-025-65906-6 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:16:y:2025:i:1:d:10.1038_s41467-025-65906-6

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-025-65906-6

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().