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Cellular immunotherapy represents a pivotal treatment modality in clinical practice. Regulatory B cells (Bregs), a key subset of B lymphocytes, hold promise in the management of autoimmune diseases, cancer and transplantation immunity. The expansion of Bregs for cell therapy is a promising strategy to alleviate inflammation and promote immune tolerance. Achieving immune tolerance relies on balance between regulatory and effector cells. One primary objective of cellular therapy is to shift this balance towards Bregs, fostering a more tolerant immune microenvironment. The adoptive transfer of Bregs not only increases their quantity but also modulates the number and function of other immune cells. Maximizing expansion of Bregs and enhancing their regulatory functions are key focuses in transplant immunology. However, the precise mechanisms underlying the expansion of IL‑10‑secreting B cells (B10) remain inadequately understood. The present review aims to provide a comprehensive overview of the signaling pathways involved in B10 activation and expansion, as well as to highlight the techniques for amplification and development of adoptive B10 therapy in transplantation, which aims to advance the field of cellular therapy targeting Bregs.
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http://dx.doi.org/10.3892/ijmm.2024.5470 | DOI Listing |
Int Immunopharmacol
August 2025
Research Unit for Pathogenic Mechanisms of Zoonotic Parasites of Chinese Academy of Medical Sciences, Key Laboratory of Livestock Infectious Diseases, Ministry of Education, Key Laboratory of Ruminant Infectious Disease Prevention and Control (East), Ministry of Agriculture and Rural Affairs, Colleg
Augmented regulatory B cell (Breg) responses are commonly observed in malaria; however, the specific parasite components and Breg subtypes involved remain unclear. In this study, we investigated C57BL/6 mice infected with Plasmodium berghei ANKA, which induces cerebral malaria pathology, in comparison to P. yoelii YM, which does not.
View Article and Find Full Text PDFTher Adv Neurol Disord
August 2025
Neuroimmunology Unit, Department of Neurosciences, Hospital Alemán, Av Pueyrredón 1640, C1118AAT, Buenos Aires, Argentina.
Neuromyelitis optica spectrum disorder (NMOSD) and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) are autoimmune diseases characterized by immune-mediated damage to the central nervous system. Current treatments primarily focus on chronic immunosuppression. Immune tolerance induction offers a novel approach to restoring immune balance while minimizing systemic side effects.
View Article and Find Full Text PDFFront Immunol
July 2025
Guangxi Clinical Research Center for Anesthesiology, Guangxi Medical University Cancer Hospital, Nanning, China.
Background: Regulatory B cells (Breg) critically orchestrate inflammatory resolution and tissue repair. This study investigates the therapeutic potential of transforming growth factor (TGF)-β1-producing Bregs in ventilator-induced lung injury (VILI), leveraging biomimetic nanotechnology to overcome limitations of conventional cytokine delivery.
Methods: We engineered macrophage-derived microvesicle-encapsulated nanoparticles (TMNP) for pH-responsive, spatiotemporally controlled TGF-β1 release.
Cell Rep
July 2025
Department of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA. Electronic address:
In B cells, BLIMP1 is required for plasma cell differentiation. BLIMP1 is also expressed in some germinal center (GC) B cells (GCBC), yet the role of BLIMP1 in GCBC is not understood. Here we generated mixed bone marrow (BM) chimeric mice using Prdm1 CD19 and Prdm1 CD19 BM, allowing us to examine the cell-intrinsic functions of BLIMP1 in GCBC, independent of antibody or antigen levels.
View Article and Find Full Text PDFJ Neuroimmunol
September 2025
Department of Pediatrics, Medical University of South Carolina, Charleston, SC, USA; Research Service, Ralph H. Johnson Veterans Administration Medical Center, Charleston, SC, USA. Electronic address:
We previously reported that S-nitrosoglutathione (GSNO) and GSNO reductase inhibitors, which increase endogenous GSNO, mitigate T cell-dependent experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis, by suppressing Th1 and Th17 effector T cells while promoting regulatory T cells (Tregs). In this study, we demonstrate that the GSNO reductase inhibitor (N6022) also alleviates B cell-dependent EAE in C57BL/6 mice immunized with recombinant human myelin oligodendrocyte glycoprotein (rhMOG). Daily N6022 treatment following disease onset significantly reduced clinical EAE disease symptoms.
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