Interleukin 10 (IL-10)-producing regulatory B-cells (Bregs) suppress inflammatory responses that mediate autoimmune diseases. However, it is unknown whether Bregs derive from a pre-existing dedicated B-cell lineage or if any B-cell can differentiate into Bregs in response to BCR or TLR activation. GL7(+) B-cells are antigen-experienced differentiated B-cells while GL7(-/lo) are at an early stage of B-cell differentiation. While both GL7(-/lo) and GL7(+) B cells can produce IL-10, differentiation of GL7(-) B-cells into Bregs does not require CD19- or Bcl6-induced signals, suggesting that BCR-induced proliferation or Ig class-switching is not necessary for generation of Breg cells. Of particular importance, we show that GL7(-) Breg cells are dramatically expanded in lupus-like mice and GL7(-) Bregs suppressed inflammatory responses in lupus-like mice by inducing expansion of Foxp3(+)Treg cells. Taken together, these results suggest that pre-existing GL7(-)IL-10(+) cells are expanded during inflammation, differentiate into GL7(+) Bregs and contribute to immune-regulation in lupus-like mice.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11315234 | PMC |
| http://dx.doi.org/10.1016/j.molimm.2016.01.011 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
A retrospective analysis of autoimmune hemolytic anemia after allogeneic hematopoietic stem cell transplantation for transfusion-dependent β-thalassemia: focus on T and B lymphocyte reconstitution.
Ann Hematol
January 2025
Department of Hematology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325035, China.
Background: Autoimmune hemolytic anemia (AIHA) following allogeneic hematopoietic stem cell transplantation (allo-HSCT) is often refractory and relapsing, leading to increased mortality post-HSCT.
Methods: We retrospectively analyzed the cases of patients with transfusion-dependent β-thalassemia (TDT) who underwent allo-HSCT to study their clinical features, the occurrence of AIHA post-HSCT, and treatment response and to explore the possible pathogenesis of AIHA.
Result: A total of 113 patients were registered in the study, out of whom 14 developed AIHA following allo-HSCT, resulting in a cumulative incidence of 12.
Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
University of Melbourne, Parkville, VIC, Australia.
Background: Mounting evidence support the involvement of adaptive immune system in the pathogenesis of Alzheimer's disease (AD). The current study investigated the age-dependent changes in the abundance of B and T cell subtypes in APP/PS1 mice, a commonly used model for AD.
Method: Peripheral blood was collected through cardiac puncture from 6-, 9-, 12-month-old APP/PS1 transgenic (TG) mice (APPsw and PSEN1dE9, n = 8-12) and their wildtype (WT) littermates (C57BL/6J, n = 12-15).
Galectin 9 rescues the inducibility of IL-10 expression in regulatory B cells of patients with food allergy.
Sci Rep
January 2025
Department of Gastroenterology, Fifth Affiliated Hospital, Zhengzhou University, Zhengzhou, China.
The deregulation of immune responses is what causes food allergy (FA) to occur. FA's cause is still unknown. The goal of this study is to investigate the mechanism how the impaired production of IL-10 occurs in peripheral naive B cells of patients with FA.
View Article and Find Full Text PDFLiver B Cells Promotes MASLD Progression via the Apelin/APLNR System.
Int J Med Sci
January 2025
Department of Medical Laboratory Science, The Third Xiangya Hospital, Central South University, Changsha, Hunan, China.
Investigate the role of the apelin/APLNR axis in metabolic dysfunction-associated steatotic liver disease (MASLD), focusing on the progression from metabolic dysfunction-associated simple steatotic liver (MASS) to metabolic dysfunction-associated steatohepatitis (MASH) and fibrosis, with emphasis on liver B cells. Serum samples from MASLD patients and liver tissues from hepatocellular carcinoma patients were collected to measure apelin and APLNR protein expression. C57BL/6J mouse models of varying MASLD stages were developed using a high-fat diet and CCl.
View Article and Find Full Text PDFCD154 blockade effectively controls antibody-mediated rejection in highly sensitized nonhuman primate kidney transplant recipients.
Sci Transl Med
January 2025
Duke Transplant Center, Department of Surgery, Duke University Medical Center, Durham, NC 27710, USA.
Current desensitization and maintenance immunosuppression regimens for kidney transplantation in sensitized individuals show limited ability to control the posttransplant humoral response, resulting in high rates of antibody-mediated rejection (ABMR) and graft failure. Here, we showed that anti-CD154 monoclonal antibody (mAb)-based immunosuppression more effectively controlled allograft rejection and humoral rebound in a highly sensitized nonhuman primate kidney transplantation model compared with tacrolimus-based standard-of-care (SOC) immunosuppression. Desensitization with an anti-CD154 mAb (5C8) and a proteasome inhibitor led to decreased donor-specific antibodies (DSAs) and disruption of lymph node germinal centers with reduction of proliferating, memory, and class-switched B cells as well as T follicular helper cells.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!