ArticleThe Journal of experimental medicine2016
B cell IFN-γ receptor signaling promotes autoimmune germinal centers via cell-intrinsic induction of BCL-6.
Article in The Journal of experimental medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 143 papers.
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Who cites it
143 citing papers in PubMed, 211 citations in OpenAlex.
- A plausibly causal functional lupus-associated risk variant in the STAT1-STAT4 locus.Human molecular genetics · 2018Trial
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- Tonsillar expression quantitative trait loci verify and expand genetic contributors to childhood atopic diseases.bioRxiv : the preprint server for biology · 2026Article
- IFNγ-induced IRF1 synergizes with TLR7 signals to tune the IRF4-IRF8 axis and drive pathogenic effector B cell fate.bioRxiv : the preprint server for biology · 2026Article
- Spatial compartmentalization shapes distinct germinal center states during respiratory viral infection.Frontiers in immunology · 2026Article
- IRF4 Promotes Immune Evasion and Shapes the Tumor Microenvironment in Follicular Lymphoma.Blood cancer discovery · 2025Article
- In Vivo Response of γδ T Cells and Macrophages to Non-Bilayer Phospholipid Arrangements in a Lupus-like Mouse Model.International journal of molecular sciences · 2025Article
- Immune Modulatory Effects of PD-1/PD-L1 in Myasthenia Gravis: Insights From Peripheral Blood Mononuclear Cell Analysis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Autoantibodies in Systemic Lupus Erythematosus: Diagnostic and Pathogenic Insights.Journal of clinical medicine · 2025Review
- Article
- IRF7 controls spontaneous autoimmune germinal center and plasma cell checkpoints.The Journal of experimental medicine · 2025Article
- Coordinated Regulation of Extrafollicular B Cell Responses by IL-12 and IFNγ.Immunological reviews · 2025Review
- The influence of the gut microbiota on B cells in autoimmune diseases.Molecular medicine (Cambridge, Mass.) · 2025Review
- T-Follicular Helper Cells and Their Role in Autoimmune Diseases.Life (Basel, Switzerland) · 2025Review
- Impact of age, HIV1, sickle-cell genotypes, and interferon-gamma gene upstream variants on malaria disease outcomes in a longitudinal pediatric cohort.Scientific reports · 2025Article
- Systems immunology analysis of human immune organoids identifies host-specific correlates of protection to different influenza vaccines.Cell stem cell · 2025Article
- Immune metabolic restoration in systemic lupus erythematosus: the impact of gut microbiota, probiotics, and nutritional synergy.Frontiers in immunology · 2025Review
- IFN-gamma in the tumor microenvironment: dual roles in cancer progression and therapy.EXCLI journal · 2025Review
- Activated B cells modulate the maturation of MDSCs via CD36-dependent MHC-II transfer to orchestrate CD4International journal of biological sciences · 2025Article
- Article
83 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Dysregulated germinal center (GC) responses are implicated in the pathogenesis of human autoimmune diseases, including systemic lupus erythematosus (SLE). Although both type 1 and type 2 interferons (IFNs) are involved in lupus pathogenesis, their respective impacts on the establishment of autoimmune GCs has not been addressed. In this study, using a chimeric model of B cell-driven autoimmunity, we demonstrate that B cell type 1 IFN receptor signals accelerate, but are not required for, lupus development. In contrast, B cells functioning as antigen-presenting cells initiate CD4(+) T cell activation and IFN-γ production, and strikingly, B cell-intrinsic deletion of the IFN-γ receptor (IFN-γR) abrogates autoimmune GCs, class-switched autoantibodies (auto-Abs), and systemic autoimmunity. Mechanistically, although IFN-γR signals increase B cell T-bet expression, B cell-intrinsic deletion of T-bet exerts an isolated impact on class-switch recombination to pathogenic auto-Ab subclasses without impacting GC development. Rather, in both mouse and human B cells, IFN-γ synergized with B cell receptor, toll-like receptor, and/or CD40 activation signals to promote cell-intrinsic expression of the GC master transcription factor, B cell lymphoma 6 protein. Our combined findings identify a novel B cell-intrinsic mechanism whereby IFN signals promote lupus pathogenesis, implicating this pathway as a potential therapeutic target in 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.