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© 2025 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.

Abstract

Rheumatoid arthritis (RA) is a systemic inflammatory autoimmune disease. The pathomechanism of RA depends on both B and T cells. Regulatory B cells (Breg) have been shown to suppress T-cell immune responses and play a key role in modulating autoimmune processes. We aimed to investigate the possibility of utilizing PD-L1+ Breg cells in downregulating the Th cells’ immune response in healthy individuals and RA patients. We hypothesized that the PD-1/PD-1L interaction plays a key role in this process, which may be defective in autoimmune diseases. We separated T and B cells from the peripheral blood of healthy volunteers and RA patients by magnetic cell sorting, and Th cells and Treg cells were isolated by fluorescence-activated cell sorting. The cytokine production by CD4+ Th cells was detected by intracellular flow cytometry. CpG and CD40L stimulations were applied to induce PD-L1hi expressing Breg cells. We found that the frequency of PD-L1hi cells is significantly lower in all B-cell subsets in RA compared to healthy controls. Functional analysis of induced PD-L1+ Breg cells in coculture with activated autologous Th cells has shown that healthy control samples containing higher levels of PD-L1hi Breg cells significantly inhibit IFN-ү and IL-21 production by Th cells. In contrast, RA patients’ samples with lower levels of PD-L1hi Breg cells failed to do so. Since the expression of PD-L1 on B cells can be modulated in vitro to induce Breg cell suppressive capacity, these data may provide new perspectives for future therapy for RA.

Details

Title
PD-L1+ Regulatory B Cells from Rheumatoid Arthritis Patients Have Impaired Function in Suppressing IFN-ү and IL-21 Production
Author
Talib, Mustafa 1   VIAFID ORCID Logo  ; Gyebrovszki, Balázs 1   VIAFID ORCID Logo  ; Fodor, Anna 1   VIAFID ORCID Logo  ; Mészáros, Anna 1 ; Kata Balog Virág 1   VIAFID ORCID Logo  ; Barta, Leila Gloria 1 ; Rojkovich, Bernadette 2 ; Nagy, György 3 ; Sármay, Gabriella 1 

 Department of Immunology, Eötvös Loránd University, 1053 Budapest, Hungary; [email protected] (M.T.); [email protected] (B.G.); [email protected] (A.F.); [email protected] (A.M.); [email protected] (L.G.B.) 
 Rheumatology-Rehabilitation Department, Buda Hospital of the Hospitaller Order of Saint John of God, 1027 Budapest, Hungary; [email protected] 
 Department of Rheumatology and Immunology, Semmelweis University, 1023 Budapest, Hungary; [email protected]; Heart and Vascular Center, Semmelweis University, 1122 Budapest, Hungary; Department of Genetics, Cell- and Immunobiology, Semmelweis University, 1089 Budapest, Hungary 
First page
2998
Publication year
2025
Publication date
2025
Publisher
MDPI AG
ISSN
16616596
e-ISSN
14220067
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
3188856823
Copyright
© 2025 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.