ArticleThe Journal of clinical investigation2005
Autoantigen, innate immunity, and T cells cooperate to break B cell tolerance during bacterial infection.
Article in The Journal of clinical investigation, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 67 citations in OpenAlex.
- Activated polyreactive B cells are clonally expanded in autoantibody positive and patients with recent-onset type 1 diabetes.Cell reports · 2025Article
- Article
- Islet-antigen reactive B cells display a unique phenotype and BCR repertoire in autoantibody positive and recent-onset type 1 diabetes patients.bioRxiv : the preprint server for biology · 2024Article
- Anti-cytokine autoantibodies: mechanistic insights and disease associations.Nature reviews. Immunology · 2024Review
- Microbes and Mental Illness: Past, Present, and Future.Healthcare (Basel, Switzerland) · 2023Review
- The oral microbiome in autoimmune diseases: friend or foe?Journal of translational medicine · 2023Review
- Differential effects of periodontal microbiome on the rheumatoid factor induction during rheumatoid arthritis pathogenesis.Scientific reports · 2022Article
- Immune Response toCurrent issues in molecular biology · 2021Article
- Modulation of Natural HLA-B*27:05 Ligandome by Ankylosing Spondylitis-associated Endoplasmic Reticulum Aminopeptidase 2 (ERAP2).Molecular & cellular proteomics : MCP · 2020Article
- Triggers of inflammatory myopathy: insights into pathogenesis.Discovery medicine · 2018Review
- The Immune Response and the Pathogenesis of Idiopathic Inflammatory Myositis: a Critical Review.Clinical reviews in allergy & immunology · 2017Review
- Autoimmune response to transthyretin in juvenile idiopathic arthritis.JCI insight · 2016Article
- How Rheumatoid Arthritis Can Result from Provocation of the Immune System by Microorganisms and Viruses.Frontiers in microbiology · 2016Review
- Autoimmune reactivity against precursor form of desmoglein 1 in healthy Tunisians in the area of endemic pemphigus foliaceus.Journal of dermatological science · 2013Article
- Carabin deficiency in B cells increases BCR-TLR9 costimulation-induced autoimmunity.EMBO molecular medicine · 2012Article
- Toll-like receptor agonists synergize with CD40L to induce either proliferation or plasma cell differentiation of mouse B cells.PloS one · 2011Article
- TLR-mediated B cell activation results in ectopic CLIP expression that promotes B cell-dependent inflammation.Journal of leukocyte biology · 2010Article
- Anti-neural antibody reactivity in patients with a history of Lyme borreliosis and persistent symptoms.Brain, behavior, and immunity · 2010Article
- Antibodies to the desmoglein 1 precursor proprotein but not to the mature cell surface protein cloned from individuals without pemphigus.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- MyD88 negatively controls hypergammaglobulinemia with autoantibody production during bacterial infection.Infection and immunity · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autoantibody production during infections is considered to result from nonspecific activation of low-affinity autoreactive B cells. Whether this can lead to autoimmune disease remains uncertain. We show that chronic infection by Borrelia burgdorferi of Tg animals expressing human rheumatoid factor (RF) B cells (of low or intermediate affinities) in the absence or in the constitutive presence of the autoantigen (represented here by chimeric IgG with human constant region) breaks their state of immunological ignorance, leading to the production of RFs. Surprisingly, this production was more pronounced in intermediate-affinity RF Tg mice co-expressing the autoantigen. This overproduction was mediated by immune complexes and involved synergistic signaling between the B cell receptor and Toll-like receptors and T cell help. These findings indicate that chronic infection can activate autoreactive B cells with significant affinity and creates conditions that can drive them to differentiate into memory cells. Such cells may have some physiological yet undetermined role, but in autoimmune-prone individuals, this scenario may initiate autoimmunity.
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.