ArticleImmunity2016
Dendritic Cells Regulate Extrafollicular Autoreactive B Cells via T Cells Expressing Fas and Fas Ligand.
Article in Immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Coordinated Regulation of Extrafollicular B Cell Responses by IL-12 and IFNγ.Immunological reviews · 2025Review
- Revealing the role of regulatory b cells in cancer: development, function and treatment significance.Cancer immunology, immunotherapy : CII · 2025Review
- Animal models of lupus nephritis: the past, present and a future outlook.Autoimmunity · 2024Review
- IgDAging cell · 2022Article
- Targeting TNature immunology · 2022Review
- PIK3IP1 Promotes Extrafollicular Class Switching in T-Dependent Immune Responses.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Immune disorder in endometrial cancer: Immunosuppressive microenvironment, mechanisms of immune evasion and immunotherapy.Oncology letters · 2020Review
- Transcriptomic and Network Analysis of Minor Salivary Glands of Patients With Primary Sjögren's Syndrome.Frontiers in immunology · 2020Article
- Cross-Reactive Antigen Expressed by B6 Splenocytes Drives Receptor Editing and Marginal Zone Differentiation of IgG2a-Reactive AM14 Vκ8 B Cells.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Bioactive Constituents ofMolecules (Basel, Switzerland) · 2019Article
- Multifaceted Role of the Placental Growth Factor (PlGF) in the Antitumor Immune Response and Cancer Progression.International journal of molecular sciences · 2019Review
- Study of the cytological features of bone marrow mesenchymal stem cells from patients with neuromyelitis optica.International journal of molecular medicine · 2019Article
- SUMO-defective c-Maf preferentially transactivates Il21 to exacerbate autoimmune diabetes.The Journal of clinical investigation · 2018Article
- Plasma Cell Differentiation Pathways in Systemic Lupus Erythematosus.Frontiers in immunology · 2018Review
- An update on lupus animal models.Current opinion in rheumatology · 2017Review
- Adoptive transfer of autoimmune splenic dendritic cells to lupus-prone mice triggers a B lymphocyte humoral response.Immunologic research · 2017Article
- Induction of Peripheral Tolerance in Ongoing Autoimmune Inflammation Requires Interleukin 27 Signaling in Dendritic Cells.Frontiers in immunology · 2017Article
- Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The extrafollicular (EF) plasmablast response to self-antigens that contain Toll-like receptor (TLR) ligands is prominent in murine lupus models and some bacterial infections, but the inhibitors and activators involved have not been fully delineated. Here, we used two conventional dendritic cell (cDC) depletion systems to investigate the role of cDCs on a classical TLR-dependent autoreactive EF response elicited in rheumatoid-factor B cells by DNA-containing immune complexes. Contrary to our hypothesis, cDC depletion amplified rather than dampened the EF response in Fas-intact but not Fas-deficient mice. Further, we demonstrated that cDC-dependent regulation requires Fas and Fas ligand (FasL) expression by T cells, but not Fas expression by B cells. Thus, cDCs activate FasL-expressing T cells that regulate Fas-expressing extrafollicular helper T (Tefh) cells. These studies reveal a regulatory role for cDCs in B cell plasmablast responses and provide a mechanistic explanation for the excess autoantibody production observed in Fas deficiency.
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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.