ArticleFrontiers in immunology2018
Interleukin-33 Contributes Toward Loss of Tolerance by Promoting B-Cell-Activating Factor of the Tumor-Necrosis-Factor Family (BAFF)-Dependent Autoantibody Production.
Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Targeting IL-33 and TSLP: A Novel Approach to Modulate Type 2 and Non-Type 2 Inflammatory Pathways in Pemphigus Vulgaris.Clinical reviews in allergy & immunology · 2026Review
- Beyond the alarm: unveiling the multifaceted role of IL-33 in kidney disease.Frontiers in immunology · 2026Review
- IL-33 expands plasma cells, disrupts germinal centers, and increases autoantibody production in mice.Nature communications · 2025Article
- Spatial Transcriptomics Resolve an Emphysema-Specific Lymphoid Follicle B Cell Signature in Chronic Obstructive Pulmonary Disease.American journal of respiratory and critical care medicine · 2024Article
- Diagnostic Evaluation Using Salivary Gland Ultrasonography in Primary Sjögren's Syndrome.Journal of clinical medicine · 2023Article
- Low Serum BAFF Concentration Is Associated with Response to TNF Inhibitors in Seropositive Patients with Rheumatoid Arthritis.Journal of clinical medicine · 2022Article
- Involvement of IL-33 in the Pathophysiology of Systemic Lupus Erythematosus: Review.International journal of molecular sciences · 2022Review
- High-throughput identification of autoantibodies that target the human exoproteome.Cell reports methods · 2022Article
- Dysregulated B cell function and disease pathogenesis in systemic sclerosis.Frontiers in immunology · 2022Review
- Article
- NETs decorated with bioactive IL-33 infiltrate inflamed tissues and induce IFN-α production in patients with SLE.JCI insight · 2021Article
- Cloning and functional testing of rhesus macaque (Macaca mulatta) IL-9 and IL-33.Journal of medical primatology · 2020Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Breaking tolerance is a key event leading to autoimmunity, but the exact mechanisms responsible for this remain uncertain. Here we show that the alarmin IL-33 is able to drive the generation of autoantibodies through induction of the B cell survival factor BAFF. A temporary, short-term increase in IL-33 results in a primary (IgM) response to self-antigens. This transient DNA-specific autoantibody response was dependent on the induction of BAFF. Notably, radiation resistant cells and not myeloid cells, such as neutrophils or dendritic cells were the major source of BAFF and were critical in driving the autoantibody response. Chronic exposure to IL-33 elicited dramatic increases in BAFF levels and resulted in elevated numbers of B and T follicular helper cells as well as germinal center formation. We also observed class-switching from an IgM to an IgG DNA-specific autoantibody response. Collectively, the results provide novel insights into a potential mechanism for breaking immune-tolerance via IL-33-mediated induction of BAFF.
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