ArticleThe Journal of investigative dermatology2015
Persistence of anti-desmoglein 3 IgG(+) B-cell clones in pemphigus patients over years.
Article in The Journal of investigative dermatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
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Who cites it
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 98 citations in OpenAlex.
- B-cell centrality dictates therapeutic efficacy across autoimmune diseases: a systematic review.Frontiers in immunology · 2026Pooled it
- Rituximab remodels the circulating immune landscape in pemphigus vulgaris revealed by high-dimensional immune profiling.Journal of translational autoimmunity · 2026Article
- Complete remission after rituximab therapy of pemphigus: Real-world evidence on dosing regimens and retreatment strategies.JID innovations : skin science from molecules to population health · 2026Article
- Clinical progress of engineered cellular immunotherapies for autoimmunity.Nature biotechnology · 2026Review
- Roads and detours for CAR T cell therapy in autoimmune diseases.Nature reviews. Drug discovery · 2026Review
- Unraveling the autoimmune architecture of pemphigus: from B-cell depletion to network-based immune engineering.Frontiers in immunology · 2026Review
- Antigen-Fc fusion therapy reduces severity of a model of pemphigus vulgaris without systemic immunosuppression.Science translational medicine · 2025Article
- Autoimmune bullous diseases: pathogenesis and clinical management.Molecular biomedicine · 2025Review
- Pemphigus relapse: Mechanisms, risk factors, and agents associated with disease recurrence.The Journal of dermatology · 2024Review
- Mechanisms of Resistance to Rituximab Used for the Treatment of Autoimmune Blistering Diseases.Life (Basel, Switzerland) · 2024Review
- Engineering chimeric autoantibody receptor T cells for targeted B cell depletion in multiple sclerosis model: AnHeliyon · 2023Article
- B-cell targeted therapy of pemphigus.The Journal of dermatology · 2023Review
- Blocking soluble Fas Ligand ameliorates pemphigus: PC111 efficacy in ex-vivo human pemphigus models.Frontiers in immunology · 2023Article
- Mouse models of pemphigus: valuable tools to investigate pathomechanisms and novel therapeutic interventions.Frontiers in immunology · 2023Review
- Temporal Outcomes after Rituximab Therapy for Pemphigus Vulgaris.The Journal of investigative dermatology · 2022Article
- Pemphigus and Pemphigoid: From Disease Mechanisms to Druggable Pathways.The Journal of investigative dermatology · 2022Review
- Role of Rituximab in the Treatment of Pemphigus Vulgaris: Patient Selection and Acceptability.Patient preference and adherence · 2022Review
- Immunotherapy for Pemphigus: Present and Future.Frontiers in medicine · 2022Review
- Current Strategies to Modulate Regulatory T Cell Activity in Allergic Inflammation.Frontiers in immunology · 2022Review
- Electron microscopy of desmosomal structures in the pemphigus human skin organ culture model.Frontiers in medicine · 2022Article
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7 authors at 2 institutions in 1 country.
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Abstract
Pemphigus vulgaris (PV) is a prototypic tissue-specific autoantibody-mediated disease, in which anti-desmoglein 3 (Dsg3) IgG autoantibodies cause life-threatening blistering. We characterized the autoimmune B-cell response over 14 patient years in two patients with active and relapsing disease, then in one of these patients after long-term remission induced by multiple courses of rituximab (anti-CD20 antibody). Characterization of the anti-Dsg3 IgG(+) repertoire by antibody phage display (APD) and PCR indicated that six clonal lines persisted in patient 1 (PV3) over 5.5 years, with only one new clone detected. Six clonal lines persisted in patient 2 (PV1) for 4 years, of which five persisted for another 4.5 years without any new clones detected. However, after long-term clinical and serologic remission, ∼11 years after initial characterization, we could no longer detect any anti-Dsg3 clones in PV1 by APD. Similarly, in another PV patient, ∼4.5 years after a course of rituximab that induced long-term remission, anti-Dsg3 B-cell clones were undetectable. These data suggest that in PV a given set of non-tolerant B-cell lineages causes autoimmune diseases and that new sets do not frequently or continually escape tolerance. Therapy such as rituximab, aimed at eliminating these aberrant sets of lineages, may be effective for disease because new ones are unlikely to develop.
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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.