ArticleAutoimmunity2012
Activation-induced deaminase contributes to the antibody-independent role of B cells in the development of autoimmunity.
Article in Autoimmunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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Who cites it
6 citing papers in PubMed.
- Activation-induced cytidine deaminase deficiency accelerates autoimmune diabetes in NOD mice.JCI insight · 2018Article
- Aberrant expression of interleukin-10 and activation-induced cytidine deaminase in B cells from patients with Behçet's disease.Biomedical reports · 2017Article
- Novel Implications in Molecular Diagnosis of Lynch Syndrome.Gastroenterology research and practice · 2017Review
- Autoimmunity in 2012.Clinical reviews in allergy & immunology · 2013Review
- Potential roles of activation-induced cytidine deaminase in promotion or prevention of autoimmunity in humans.Autoimmunity · 2013Review
- Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
B cells contribute to autoimmunity both as secretors of pathogenic antibodies and through the activation of autoreactive T cells. B cells and antibodies acquire higher affinity to self-antigen through a process known as immunoglobulin hypermutation or SHM. The contribution of SHM to pathogenic antibody development in lupus has been established in various autoimmune mouse models and by examining antibodies from patients. However, its role in the antibody-independent contribution of B cells to autoimmunity has not been examined. Herein, we generate lupus-prone MRL/lpr mice with a limited IgM-only B cell repertoire, no secreted antibodies and no SHM. This enabled us to isolate the role of somatic hypermutation in B cell-mediated autoimmunity. We found that SHM-deficiency correlated with a reduction in autoreactive B cells, a decrease in T cell activation and a decrease in kidney lymphocytic infiltration. These data establish AID as an important contributor to the antibody-independent role of B cells in autoimmunity.
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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.