ArticleThe Journal of experimental medicine2016
IFN-γ receptor and STAT1 signaling in B cells are central to spontaneous germinal center formation and autoimmunity.
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 128 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
128 citing papers in PubMed, 198 citations in OpenAlex.
- Proteins linked to type II interferon response in Sjögren's disease: novel indicators for disease monitoring and predicting treatment response to leflunomide and hydroxychloroquine combination therapy.Frontiers in immunology · 2025Trial
- Immunometabolism and rheumatic disease-advancing targeted therapies.EULAR rheumatology open · 2026Review
- Gastric cancer tertiary lymphoid structures in the muscularis propria are associated with therapy resistance and promote immunosuppression.Nature communications · 2026Article
- Ptpn2 limits plasma cell fate and antiviral immunity by integrating B cell receptor and IFN-γ signals in B cells.Science advances · 2026Article
- Progressive deterioration of adaptive immune repertoires in Down syndrome linked to interferon hyperactivity and lymphoid tissue disorganization.bioRxiv : the preprint server for biology · 2026Article
- WASH regulates B cell signaling, metabolism and function through STAT1.Cell death and differentiation · 2026Article
- IFN-γ and TLR agonist co-adjuvants enhance the efficacy of a lipid-PLGA hybrid nanoparticle-based oxycodone vaccine.Biomaterials · 2026Article
- The landscape of B and plasma cells in breast cancer: insights from single-cell and spatial transcriptomics.NPJ breast cancer · 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
- Immunopathogenesis and Therapeutics of Systemic Lupus Erythematosus: an Integrative Review.Clinical reviews in allergy & immunology · 2025Review
- IRF4 Promotes Immune Evasion and Shapes the Tumor Microenvironment in Follicular Lymphoma.Blood cancer discovery · 2025Article
- Interferon-γ receptor signaling is critical for balanced immune activation and protection against influenza after vaccination.Virology · 2025Article
- Multivariate analysis of glycogenes reveals coordinated regulation of immunoglobulin glycosylation in an immortalized human B cell system.bioRxiv : the preprint server for biology · 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
- HybriSeq: probe-based device-free single-cell RNA profiling.Communications biology · 2025Article
- Article
- T-bet+ CXCR3+ B cells drive hyperreactive B-T cell interactions in multiple sclerosis.Cell reports. Medicine · 2025Article
- Follicle-like niches outside the cortex? 3D phase-contrast µCT revealed medullary B cell nodules in mucosa-draining lymph nodes.Frontiers in immunology · 2025Article
- Liver-draining portal lymph node responds to enteric nematode infection by generating highly parasite-specific follicular T helper and B cell responses.Frontiers in immunology · 2025Article
- STAT signaling pathways in immune cells and their associated mechanisms in cancer pathogenesis.BioImpacts : BI · 2025Review
68 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Spontaneously developed germinal centers (GCs [Spt-GCs]) harbor autoreactive B cells that generate somatically mutated and class-switched pathogenic autoantibodies (auto-Abs) to promote autoimmunity. However, the mechanisms that regulate Spt-GC development are not clear. In this study, we report that B cell-intrinsic IFN-γ receptor (IFN-γR) and STAT1 signaling are required for Spt-GC and follicular T helper cell (Tfh cell) development. We further demonstrate that IFN-γR and STAT1 signaling control Spt-GC and Tfh cell formation by driving T-bet expression and IFN-γ production by B cells. Global or B cell-specific IFN-γR deficiency in autoimmune B6.Sle1b mice leads to significantly reduced Spt-GC and Tfh cell responses, resulting in diminished antinuclear Ab reactivity and IgG2c and IgG2b auto-Ab titers compared with B6.Sle1b mice. Additionally, we observed that the proliferation and differentiation of DNA-reactive B cells into a GC B cell phenotype require B cell-intrinsic IFN-γR signaling, suggesting that IFN-γR signaling regulates GC B cell tolerance to nuclear self-antigens. The IFN-γR deficiency, however, does not affect GC, Tfh cell, or Ab responses against T cell-dependent foreign antigens, indicating that IFN-γR signaling regulates autoimmune, but not the foreign antigen-driven, GC and Tfh cell responses. Together, our data define a novel B cell-intrinsic IFN-γR signaling pathway specific to Spt-GC development and autoimmunity. This novel pathway can be targeted for future pharmacological intervention to treat systemic lupus erythematosus.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.