ArticleAutoimmunity2013
Critical role of activation induced cytidine deaminase in experimental autoimmune encephalomyelitis.
Article in Autoimmunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- ODC1 restricts meningeal B cell age-associated-like phenotype and function in multiple sclerosis: A human and experimental study.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- CD40 Drives Central Nervous System Autoimmune Disease by Inducing Complementary Effector Programs via B Cells and Dendritic Cells.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Multiple sclerosis genetic and non-genetic factors interact through the transient transcriptome.Scientific reports · 2022Article
- Class switching and high-affinity immunoglobulin G production by B cells is dispensable for the development of hypertension in mice.Cardiovascular research · 2021Article
- Siponimod therapy implicates Th17 cells in a preclinical model of subpial cortical injury.JCI insight · 2020Article
- Base Excision Repair in the Immune System: Small DNA Lesions With Big Consequences.Frontiers in immunology · 2020Review
- Activation-induced cytidine deaminase deficiency accelerates autoimmune diabetes in NOD mice.JCI insight · 2018Article
- Polyclonal hyper-IgE mouse model reveals mechanistic insights into antibody class switch recombination.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- AID stabilizes stem-cell phenotype by removing epigenetic memory of pluripotency genes.Nature · 2013Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors at 1 institution.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple Sclerosis (MS) is a neurodegenerative autoimmune disorder caused by chronic inflammation and demyelination within the central nervous system (CNS). Clinical studies in MS patients have demonstrated efficacy with B cell targeted therapies such as anti-CD20. However, the exact role that B cells play in the disease process is unclear. Activation Induced cytidine deaminase (AID) is an essential enzyme for the processes of antibody affinity maturation and isotype switching. To evaluate the impact of affinity maturation and isotype switching, we have interrogated the effect of AID-deficiency in an animal model of MS. Here, we show that the severity of experimental autoimmune encephalomyelitis (EAE) induced by the extracellular domain of human myelin oligodendrocyte glycoprotein (MOG1-125) is significantly reduced in Aicda deficient mice, which, unlike wild-type mice, lack serum IgG to myelin associated antigens. MOG specific T cell responses are comparable between wild-type and Aicda knockout mice suggesting an active role for antigen experienced B cells. Thus affinity maturation and/or class switching are critical processes in the pathogenesis of EAE.
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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.