ArticleJournal of immunology (Baltimore, Md. : 1950)2020
Serine Phosphorylation of the STAT1 Transactivation Domain Promotes Autoreactive B Cell and Systemic Autoimmunity Development.
Article in Journal of immunology (Baltimore, Md. : 1950), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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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.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- STAT Signaling and Its Anti-Apoptotic Effects in Dehydrated Xenopus laevis.Biology of the cell · 2026Article
- The microbiota-systemic lupus erythematosus axis: mechanisms, diagnostics, and therapeutic frontiers.Frontiers in immunology · 2026Review
- Tracking clonal dynamics of CD8 T cells and immune dysregulation in progression of systemic lupus erythematosus with nephritis.Experimental & molecular medicine · 2025Article
- IRF7 controls spontaneous autoimmune germinal center and plasma cell checkpoints.The Journal of experimental medicine · 2025Article
- The influence of the gut microbiota on B cells in autoimmune diseases.Molecular medicine (Cambridge, Mass.) · 2025Review
- Mechanical sensing protein PIEZO1 controls osteoarthritis via glycolysis mediated mesenchymal stem cells-Th17 cells crosstalk.Cell death & disease · 2025Article
- Transcription Factors in the Pathogenesis of Lupus Nephritis and Their Targeted Therapy.International journal of molecular sciences · 2024Review
- Case report: A novelFrontiers in immunology · 2024Article
- STAT3 signaling in B cells controls germinal center zone organization and recycling.Cell reports · 2023Article
- Review
- Regulation of B Cell Responses in SLE by Three Classes of Interferons.International journal of molecular sciences · 2021Review
- STAT4 Is Largely Dispensable for Systemic Lupus Erythematosus-like Autoimmune- and Foreign Antigen-Driven Antibody-Forming Cell, Germinal Center, and Follicular Th Cell Responses.ImmunoHorizons · 2021Article
- Mechanism of Follicular Helper T Cell Differentiation Regulated by Transcription Factors.Journal of immunology research · 2020Review
- Recent Advances in Lupus B Cell Biology: PI3K, IFNγ, and Chromatin.Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 3 countries.
Funding
Abstract
Although STAT1 tyrosine-701 phosphorylation (designated STAT1-pY701) is indispensable for STAT1 function, the requirement for STAT1 serine-727 phosphorylation (designated STAT1-pS727) during systemic autoimmune and antipathogen responses remains unclear. Using autoimmune-prone B6.Sle1b mice expressing a STAT1-S727A mutant in which serine is replaced by alanine, we report in this study that STAT1-pS727 promotes autoimmune Ab-forming cell (AFC) and germinal center (GC) responses, driving autoantibody production and systemic lupus erythematosus (SLE) development. In contrast, STAT1-pS727 is not required for GC, T follicular helper cell (Tfh), and Ab responses to various foreign Ags, including pathogens. STAT1-pS727 is also not required for gut microbiota and dietary Ag-driven GC and Tfh responses in B6.Sle1b mice. By generating B cell-specific bone marrow chimeras, we demonstrate that STAT1-pS727 plays an important B cell-intrinsic role in promoting autoimmune AFC, GC, and Tfh responses, leading to SLE-associated autoantibody production. Our analysis of the TLR7-accelerated B6.Sle1b.Yaa SLE disease model expressing a STAT1-S727A mutant reveals STAT1-pS727-mediated regulation of autoimmune AFC and GC responses and lupus nephritis development. Together, we identify previously unrecognized differential regulation of systemic autoimmune and antipathogen responses by STAT1-pS727. Our data implicate STAT1-pS727 as a therapeutic target for SLE without overtly affecting STAT1-mediated protection against pathogenic infections.
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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.