ArticleFrontiers in immunology2019
The Balance in T Follicular Helper Cell Subsets Is Altered in Neuromyelitis Optica Spectrum Disorder Patients and Restored by Rituximab.
Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 36 citations in OpenAlex.
- Decoding autoimmune disease with single-cell immune repertoire and transcriptome sequencing: mechanisms and therapeutic opportunities.Frontiers in immunology · 2026Review
- Distinct remission immune architectures under rituximab and azathioprine in AQP4-IgG-positive neuromyelitis optica spectrum disorder.Frontiers in immunology · 2026Article
- Dysregulated Tfh/B cells and their interactions in neuromyelitis optica spectrum disorder.Frontiers in immunology · 2025Article
- The Role of Gut Microbiota in Neuromyelitis Optica Spectrum Disorder.International journal of molecular sciences · 2024Review
- Clinical significance of T helper cell subsets in the peripheral blood and bone marrow of patients with multiple myeloma.Frontiers in immunology · 2024Article
- Normalized circulating Tfh and Th17 associates with improvement in myasthenia gravis treated with ofatumumab.Frontiers in immunology · 2024Article
- Renegade T cell clones and autoimmune disease.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- T follicular helper cells contribute to pathophysiology in a model of neuromyelitis optica spectrum disorders.JCI insight · 2023Article
- Immuno-pathogenesis of neuromyelitis optica and emerging therapies.Seminars in immunopathology · 2022Review
- Review
- Monoclonal Antibody Therapies Beyond Complement for NMOSD and MOGAD.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Review
- Gut Microbiome and Bile Acid Metabolism Induced the Activation of CXCR5+ CD4+ T Follicular Helper Cells to Participate in Neuromyelitis Optica Spectrum Disorder Recurrence.Frontiers in immunology · 2022Article
- Treatment of Neuromyelitis Optica Spectrum Disorders.International journal of molecular sciences · 2021Review
- Altered distributions in circulating follicular helper and follicular regulatory T cells accountable for imbalanced cytokine production in multiple sclerosis.Clinical and experimental immunology · 2021Article
- Association of Circulating T Follicular Helper Cells With Idiopathic Optic Neuritis and Neuromyelitis Optica Spectrum Disorders.Frontiers in neurology · 2021Article
- Effects of Tocilizumab Therapy on Circulating B Cells and T Helper Cells in Patients With Neuromyelitis Optica Spectrum Disorder.Frontiers in immunology · 2021Article
- Association of Circulating Follicular Helper T Cells and Serum CXCL13 With Neuromyelitis Optica Spectrum Disorders.Frontiers in immunology · 2021Article
- Emerging Targeted Therapies for Neuromyelitis Optica Spectrum Disorders.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2021Review
- Pro-inflammatory dopamine-2 receptor-specific T cells in paediatric movement and psychiatric disorders.Clinical & translational immunology · 2020Article
Corrections and comments
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Authors and funding
7 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuromyelitis optica spectrum disorder (NMOSD) is a rare and severe auto-immune disease of the central nervous system driven by pathogenic antibodies mainly directed against aquaporin-4 (AQP4-Ab). Treatment of NMOSD currently relies on immunosuppressants (mycophenolate mofetil, azathioprine) or B-cell-depleting therapy (rituximab). B-cell differentiation into antibody-producing cells requires T follicular helper cells (Tfh). There are several Tfh subsets that differentially affect B-cell differentiation; Tfh2 and Tfh17 subsets strongly support B-cell differentiation. By contrast, Tfh1 lack this capacity and T follicular regulatory cells (Tfr), inhibit B-cell differentiation into antibody-producing cells. We performed a broad characterization of circulating Tfh subsets in 25 NMOSD patients and analyzed the impact of different treatments on these subsets. Untreated NMOSD patients presented a Tfh polarization toward excessive B-helper Tfh subsets with an increase of Tfh17 and (Tfh2+Tfh17)/Tfh1 ratio and a decrease of Tfr and Tfh1. Rituximab restored the Tfh polarization to that of healthy controls. There was a trend toward a similar result for azathioprine and mycophenolate mofetil. Our results suggest that NMOSD patients present an impaired balance in Tfh subsets favoring B-cell differentiation which may explain the sustained antibody production. These findings provide new insights into the pathophysiology of NMOSD, and further suggest that Tfh and Tfr subsets could be considered as potential therapeutic target in NMOSD because of their upstream role in antibody production.
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