ArticleProceedings of the National Academy of Sciences of the United States of America2007
Subversion of B lymphocyte tolerance by hydralazine, a potential mechanism for drug-induced lupus.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 90 citations in OpenAlex.
- An Update Comprehensive Review on Epigenetic Modifications and Therapies in Autoimmune Diseases.Clinical reviews in allergy & immunology · 2026Review
- Epigenetic dysregulation of B‑cells in autoimmune diseases and lymphomas (Review).International journal of molecular medicine · 2026Review
- Article
- Cardiovascular precision medicine - A pharmacogenomic perspective.Cambridge prisms. Precision medicine · 2023Review
- Targeting epigenetic regulators for inflammation: Mechanisms and intervention therapy.MedComm · 2022Review
- Autoreactive B cells recruited to lungs by silica exposure contribute to local autoantibody production in autoimmune-prone BXSB and B cell receptor transgenic mice.Frontiers in immunology · 2022Article
- Pharmacogenetics to guide cardiovascular drug therapy.Nature reviews. Cardiology · 2021Review
- Effects of Treatment with the Hypomethylating Agent 5-aza-2'-deoxycytidine in Murine Type II Collagen-Induced Arthritis.Pharmaceuticals (Basel, Switzerland) · 2019Article
- DNA methylation as a transcriptional regulator of the immune system.Translational research : the journal of laboratory and clinical medicine · 2019Review
- The Pathogenic Role of Dysregulated Epigenetic Modifications in Autoimmune Diseases.Frontiers in immunology · 2019Review
- Article
- Drug-induced lupus erythematosus: an update on drugs and mechanisms.Current opinion in rheumatology · 2018Review
- Epigenetic regulation in B-cell maturation and its dysregulation in autoimmunity.Cellular & molecular immunology · 2018Review
- Potential Chronotherapeutic Optimization of Antimalarials in Systemic Lupus Erythematosus: Is Toll-Like Receptor 9 Expression Dependent on the Circadian Cycle in Humans?Frontiers in immunology · 2018Article
- DNA methylation alterations in the pathogenesis of lupus.Clinical and experimental immunology · 2017Review
- Epigenetic Control of B Cell Development and B-Cell-Related Immune Disorders.Clinical reviews in allergy & immunology · 2016Review
- Epigenetics of multiple sclerosis: an updated review.Neuromolecular medicine · 2015Review
- The real culprit in systemic lupus erythematosus: abnormal epigenetic regulation.International journal of molecular sciences · 2015Review
- An epigenetic view of B-cell disorders.Immunology and cell biology · 2015Review
- Epigenetics of Peripheral B-Cell Differentiation and the Antibody Response.Frontiers in immunology · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulating evidence indicates that epigenetic alterations contribute to exacerbated activation or deregulation of the mechanisms that maintain tolerance to self-antigens in patients with lupus, a systemic autoimmune disease that can be triggered by medications taken to treat a variety of conditions. Here, we tested the effect of hydralazine, an antihypertensive drug that triggers lupus, on receptor editing, a chief mechanism of B lymphocyte tolerance to self-antigens. Using mice expressing transgenic human Igs, we found that hydralazine impairs up-regulation of RAG-2 gene expression and reduces secondary Ig gene rearrangements. Receptor editing was also partially abolished in a dose-dependent manner by a specific inhibitor of MEK1/2. Adoptive transfer of bone marrow B cells pretreated with hydralazine or with a MEK inhibitor to naïve syngeneic mice resulted in autoantibody production. We conclude that, by disrupting receptor editing, hydralazine subverts B lymphocyte tolerance to self and contributes to generation of pathogenic autoreactivity. We also postulate that inhibition of the Erk signaling pathway contributes to the pathogenesis of hydralazine-induced lupus and idiopathic human lupus.
Indexed as
Identifiers
What OpenQuestion holds
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.