ArticleThe Journal of experimental medicine2009
Follicular helper T cells are required for systemic autoimmunity.
Article in The Journal of experimental medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 324 papers.
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Who cites it
324 citing papers in PubMed.
- The activity level of follicular helper T cells in the peripheral blood of osteosarcoma patients is associated with poor prognosis.Bioengineered · 2022Trial
- Exaggerated follicular helper T-cell responses in patients with LRBA deficiency caused by failure of CTLA4-mediated regulation.The Journal of allergy and clinical immunology · 2018Trial
- Gender Bias in Human Systemic Lupus Erythematosus: A Problem of Steroid Receptor Action?Frontiers in immunology · 2018Trial
- A cholinergic checkpoint controls autoantibody selection via somatic hypermutation in lupus germinal centers.Cellular & molecular immunology · 2026Article
- Defective inducible T cell costimulator signalling drives neuropilin-1Experimental & molecular medicine · 2026Article
- From Genes to Pathways: The Molecular Landscape of Systemic Lupus Erythematosus.International journal of molecular sciences · 2026Review
- [Regulatory effects of mesenchymal stem cells on B1 cells and Tfh cells in children with systemic lupus erythematosus].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026Article
- Extrafollicular and Other Non-Germinal Center B Cell Responses: An Evolutionary Perspective.Immunological reviews · 2025Review
- FXR inhibition functions as a checkpoint blockade of the pathogenic Tfh cell response in lupus.Cellular & molecular immunology · 2025Article
- Metabolic pathways within cTfh subsets and glucose-dependent activation of cTfh17 in SLE and healthy individuals.JCI insight · 2025Article
- Single-cell RNA sequencing reveals that a high salt diet increases IL6R-JAK1-STAT3 gene signaling pathway activity in intestinal B cells and Tfh cells of salt-sensitive hypertension animal model.Scientific reports · 2025Article
- Cellular therapies in rheumatic and musculoskeletal diseases.Journal of translational autoimmunity · 2025Review
- T-Follicular Helper Cells and Their Role in Autoimmune Diseases.Life (Basel, Switzerland) · 2025Review
- Predictors of Splenectomy Response in Immune Thrombocytopenia: A Multicentric Italian Study.Journal of clinical medicine · 2024Article
- Article
- CD4Nature communications · 2024Article
- ETV5 promotes lupus pathogenesis and follicular helper T cell differentiation by inducing osteopontin expression.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Metabolic imbalance driving immune cell phenotype switching in autoimmune disorders: Tipping the balance of T- and B-cell interactions.Clinical and translational medicine · 2024Article
- T cell help shapes B cell tolerance.Science immunology · 2024Article
- CaMK4 controls follicular helper T cell expansion and function during normal and autoimmune T-dependent B cell responses.Nature communications · 2024Article
264 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Production of high-affinity pathogenic autoantibodies appears to be central to the pathogenesis of lupus. Because normal high-affinity antibodies arise from germinal centers (GCs), aberrant selection of GC B cells, caused by either failure of negative selection or enhanced positive selection by follicular helper T (T(FH)) cells, is a plausible explanation for these autoantibodies. Mice homozygous for the san allele of Roquin, which encodes a RING-type ubiquitin ligase, develop GCs in the absence of foreign antigen, excessive T(FH) cell numbers, and features of lupus. We postulated a positive selection defect in GCs to account for autoantibodies. We first demonstrate that autoimmunity in Roquin(san/san) (sanroque) mice is GC dependent: deletion of one allele of Bcl6 specifically reduces the number of GC cells, ameliorating pathology. We show that Roquin(san) acts autonomously to cause accumulation of T(FH) cells. Introduction of a null allele of the signaling lymphocyte activation molecule family adaptor Sap into the sanroque background resulted in a substantial and selective reduction in sanroque T(FH) cells, and abrogated formation of GCs, autoantibody formation, and renal pathology. In contrast, adoptive transfer of sanroque T(FH) cells led to spontaneous GC formation. These findings identify T(FH) dysfunction within GCs and aberrant positive selection as a pathway to systemic autoimmunity.
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