ArticleJournal of immunology (Baltimore, Md. : 1950)2015
IFN-β treatment requires B cells for efficacy in neuroautoimmunity.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
45 citing papers in PubMed, 69 citations in OpenAlex.
- Imbalance of Circulating B-Cell Subsets Was Associated With Higher Risk of Relapses in RRMS Patients.Journal of immunology research · 2026Article
- Lactylation Genes LDHA and LDHC Alleviate Osteoarthritis by Reducing Specific B-Cell Expression: Mechanistic Exploration and Experimental Validation.Journal of cellular and molecular medicine · 2025Article
- Interferon-β treatment reverses the detrimental effect of B-cell depletion therapy on respiratory virus infection.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Human regulatory memory B cells defined by expression of TIM-1 and TIGIT are dysfunctional in multiple sclerosis.Frontiers in immunology · 2024Article
- The BAFF-APRIL System in Cancer.Cancers · 2023Review
- Dual Role of B Cells in Multiple Sclerosis.International journal of molecular sciences · 2023Review
- Under the influence: environmental factors as modulators of neuroinflammation through the IL-10/IL-10R axis.Frontiers in immunology · 2023Review
- Intrahepatic transcriptomics reveals gene signatures in chronic hepatitis B patients responded to interferon therapy.Emerging microbes & infections · 2022Article
- Targeting CD38 in Neoplasms and Non-Cancer Diseases.Cancers · 2022Review
- Activation pathways that drive CD4Immunological reviews · 2022Review
- The emerging role of regulatory cell-based therapy in autoimmune disease.Frontiers in immunology · 2022Review
- Targeting IFN activity to both B cells and plasmacytoid dendritic cells induces a robust tolerogenic response and protection against EAE.Scientific reports · 2021Article
- Inflammation in multiple sclerosis.Therapeutic advances in neurological disorders · 2021Review
- Memory B Cells in Multiple Sclerosis: Emerging Players in Disease Pathogenesis.Frontiers in immunology · 2021Review
- The Role of B Cells in Primary Progressive Multiple Sclerosis.Frontiers in neurology · 2021Review
- Regulatory B cells in respiratory health and diseases.Immunological reviews · 2021Review
- The role of B cells in the immunopathogenesis of multiple sclerosis.Immunology · 2020Review
- Differential Effects of MS Therapeutics on B Cells-Implications for Their Use and Failure in AQP4-Positive NMOSD Patients.International journal of molecular sciences · 2020Review
- Impact of cytomegalovirus infection on B cell differentiation and cytokine production in multiple sclerosis.Journal of neuroinflammation · 2020Article
- B cell function impacts the efficacy of IFN-β therapy in EAE.Journal of neuroimmunology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
IFN-β remains the most widely prescribed treatment for relapsing remitting multiple sclerosis. Despite widespread use of IFN-β, the therapeutic mechanism is still partially understood. Particularly, the clinical relevance of increased B cell activity during IFN-β treatment is unclear. In this article, we show that IFN-β pushes some B cells into a transitional, regulatory population that is a critical mechanism for therapy. IFN-β treatment increases the absolute number of regulatory CD19(+)CD24(++)CD38(++) transitional B cells in peripheral blood relative to treatment-naive and Copaxone-treated patients. In addition, we found that transitional B cells from both healthy controls and IFN-β-treated MS patients are potent producers of IL-10, and that the capability of IFN-β to induce IL-10 is amplified when B cells are stimulated. Similar changes are seen in mice with experimental autoimmune encephalomyelitis. IFN-β treatment increases transitional and regulatory B cell populations, as well as IL-10 secretion in the spleen. Furthermore, we found that IFN-β increases autoantibody production, implicating humoral immune activation in B cell regulatory responses. Finally, we demonstrate that IFN-β therapy requires immune-regulatory B cells by showing that B cell-deficient mice do not benefit clinically or histopathologically from IFN-β treatment. These results have significant implications for the diagnosis and treatment of relapsing remitting multiple sclerosis.
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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.