ArticleFrontiers in immunology2022
The extrafollicular response is sufficient to drive initiation of autoimmunity and early disease hallmarks of lupus.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 33 citations in OpenAlex.
- Targeting T follicular helper cells for lifelong health.Nature reviews. Drug discovery · 2026Review
- Epigenetic regulation of B cell tolerance and dysfunction in autoimmune disease.Nature reviews. Immunology · 2026Review
- Evolution of self-reactive B cells: lessons from a lupus model.Biochemical Society transactions · 2026Review
- Defective inducible T cell costimulator signalling drives neuropilin-1Experimental & molecular medicine · 2026Article
- Germinal-centre and extrafollicular B cell pathways in systemic lupus erythematosus.Nature reviews. Rheumatology · 2026Review
- Serial intravital microscopy reveals temporal dynamics of autoreactive germinal centers in the spleen.iScience · 2026Article
- Review
- Loss of ST8Sia6 mediated α-2,8-linked di-sialylation enhances T cell-dependent antibody responses and promotes autoimmunity in aged mice.Frontiers in immunology · 2026Article
- Distributed apoptotic checkpoints in B cell selection, tolerance, and autoimmunity.Frontiers in immunology · 2026Review
- Chronic TLR7 activation promotes expansion of activated CD11cFrontiers in immunology · 2026Article
- 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
- Innate Immune Receptors as Dynamic Modulators of Extrafollicular Autoimmune B Cell Response.Immunological reviews · 2025Review
- Signaling Activation and Modulation in Extrafollicular B Cell Responses.Immunological reviews · 2025Review
- Association between peripheral activated naive and double negative 2 B-cell subsets and clinical parameters in lupus nephritis patients.Scandinavian journal of immunology · 2025Article
- Bank1 modulates the differentiation and molecular profile of key B cell populations in autoimmunity.JCI insight · 2024Article
- Invasion of spontaneous germinal centers by naive B cells is rapid and persistent.Science immunology · 2024Article
- Lupus-associated innate receptors drive extrafollicular evolution of autoreactive B cells.bioRxiv : the preprint server for biology · 2024Article
- Germinal center versus extrafollicular responses in systemic autoimmunity: Who turns the blade on self?Advances in immunology · 2024Review
- Pathophysiological, immunological, and inflammatory features of long COVID.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Many autoimmune diseases are characterized by germinal center (GC)-derived, affinity-matured, class-switched autoantibodies, and strategies to block GC formation and progression are currently being explored clinically. However, extrafollicular responses can also play a role. The aim of this study was to investigate the contribution of the extrafollicular pathway to autoimmune disease development. Methods: We blocked the GC pathway by knocking out the transcription factor Bcl-6 in GC B cells, leaving the extrafollicular pathway intact. We tested the impact of this intervention in two murine models of systemic lupus erythematosus (SLE): a pharmacological model based on chronic epicutaneous application of the Toll-like receptor (TLR)-7 agonist Resiquimod (R848), and 564Igi autoreactive B cell receptor knock-in mice. The B cell intrinsic effects were further investigated Results: GC block failed to curb autoimmune progression in the R848 model based on anti-dsDNA and plasma cell output, superoligomeric DNA complexes, and immune complex deposition in glomeruli. The 564Igi model confirmed this based on anti-dsDNA and plasma cell output. Discussion: We identified the extrafollicular pathway as a key contributor to autoimmune progression. We propose that therapeutic targeting of low quality and poorly controlled extrafollicular responses could be a desirable strategy to curb autoreactivity, as it would leave intact the more stringently controlled and high-quality GC responses providing durable protection against infection.
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