ArticleJournal of immunology (Baltimore, Md. : 1950)2016
STAT3 Signaling in B Cells Is Critical for Germinal Center Maintenance and Contributes to the Pathogenesis of Murine Models of Lupus.
Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 79 citations in OpenAlex.
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- Building an Interleukin-10-Producing Identity: How B Cells Acquire Interleukin-10 Competence and How Plasma Cell Differentiation Consolidates This Program.Immunological reviews · 2026Review
- Phosphorylated TYK2 orchestrates the pathogenic program of CD4 + T cells in the development of CNS autoimmunity.Journal of neuroinflammation · 2026Article
- Plasmablast Storms: Microbial Drivers of Acute and Chronic Autoimmune Flares.Microorganisms · 2026Review
- Arid2 promotes Follicular B-cell differentiation and antibody responsesbioRxiv : the preprint server for biology · 2025Article
- Glutaredoxin2 reduces age-associated B cell differentiation through maintaining redox homeostasis.Frontiers in pharmacology · 2025Article
- Aberrant zonal recycling of germinal center B cells impairs appropriate selection in lupus.Cell reports · 2024Article
- Article
- Synergistic effects of BTN3A1, SHP2, CD274, and STAT3 gene polymorphisms on the risk of systemic lupus erythematosus: a multifactorial dimensional reduction analysis.Clinical rheumatology · 2024Article
- Sphingosine-1-Phosphate Receptor 4 links neutrophils and early local inflammation to lymphocyte recruitment into the draining lymph node to facilitate robust germinal center formation.Frontiers in immunology · 2024Article
- Agomir miRNA-150-5p alleviates pristane-induced lupus by suppressing myeloid dendritic cells activation and inflammation via TREM-1 axis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- STAT3 signaling in B cells controls germinal center zone organization and recycling.Cell reports · 2023Article
- B cell-intrinsic STAT3-mediated support of latency and interferon suppression during murine gammaherpesvirus 68 infection revealed through anbioRxiv : the preprint server for biology · 2023Article
- A synthetic human 3DiScience · 2023Article
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- Janus kinase inhibitors in systemic lupus erythematosus: implications for tyrosine kinase 2 inhibition.Frontiers in medicine · 2023Review
- A multi-view latent variable model reveals cellular heterogeneity in complex tissues for paired multimodal single-cell data.Bioinformatics (Oxford, England) · 2023Article
- Norcantharidin ameliorates the development of murine lupus via inhibiting the generation of IL-17 producing cells.Acta pharmacologica Sinica · 2022Article
- Interleukin-10 contributes to reservoir establishment and persistence in SIV-infected macaques treated with antiretroviral therapy.The Journal of clinical investigation · 2022Article
- Cell Type-Specific Roles of STAT3 Signaling in the Pathogenesis and Progression of K-ras Mutant Lung Adenocarcinoma.Cancers · 2022Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Ab maturation as well as memory B and plasma cell differentiation occur primarily in the germinal centers (GCs). Systemic lupus erythematosus (SLE) may develop as a result of enhanced GC activity. Previous studies have shown that the dysregulated STAT3 pathway is linked to lupus pathogenesis. However, the exact role of STAT3 in regulating SLE disease progression has not been fully understood. In this study, we demonstrated that STAT3 signaling in B cells is essential for GC formation and maintenance as well as Ab response. Increased cell apoptosis and downregulated Bcl-xL and Mcl-1 antiapoptotic gene expression were found in STAT3-deficient GC B cells. The follicular helper T cell response positively correlated with GC B cells and was significantly decreased in immunized B cell STAT3-deficient mice. STAT3 deficiency also led to the defect of plasma cell differentiation. Furthermore, STAT3 deficiency in autoreactive B cells resulted in decreased autoantibody production. Results obtained from B cell STAT3-deficient B6.MRL/lpr mice suggest that STAT3 signaling significantly contributes to SLE pathogenesis by regulation of GC reactivity, autoantibody production, and kidney pathology. Our findings provide new insights into the role of STAT3 signaling in the maintenance of GC formation and GC B cell differentiation and identify STAT3 as a novel target for treatment of SLE.
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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.