ReviewJournal of autoimmunity2013
Rethinking mechanisms of autoimmune pathogenesis.
Review in Journal of autoimmunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 68 citations in OpenAlex.
- Immune checkpoints in a genetically engineered mouse model of spontaneous autoimmune uveitis.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Spontaneous organ-specific eye autoimmune disease resulting from two engineered gene mutations compromising immune tolerance.Frontiers in immunology · 2026Review
- CPT-11 mitigates autoimmune diseases by suppressing effector T cells without affecting long-term anti-tumor immunity.Cell death discovery · 2024Article
- Gut Microbiome-Related Anti-Inflammatory Effects of Aryl Hydrocarbon Receptor Activation on Inflammatory Bowel Disease.International journal of molecular sciences · 2024Review
- Tracking the role of Aire in immune tolerance to the eye with a TCR transgenic mouse model.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The emerging role of noncoding RNAs in systemic lupus erythematosus: new insights into the master regulators of disease pathogenesis.Therapeutic advances in chronic disease · 2023Review
- Development and applications of sialoglycan-recognizing probes (SGRPs) with defined specificities: exploring the dynamic mammalian sialoglycome.Glycobiology · 2022Article
- Landscape of intestinal microbiota in patients with IgA nephropathy, IgA vasculitis and Kawasaki disease.Frontiers in cellular and infection microbiology · 2022Article
- N-Glycosylation and Inflammation; the Not-So-Sweet Relation.Frontiers in immunology · 2022Review
- Dietary Quercetin Increases Colonic Microbial Diversity and Attenuates Colitis Severity inFrontiers in microbiology · 2019Article
- The microbiome and autoimmunity: a paradigm from the gut-liver axis.Cellular & molecular immunology · 2018Review
- Exploration of the Sialic Acid World.Advances in carbohydrate chemistry and biochemistry · 2018Review
- Impact of the Gut Microbiota on Intestinal Immunity Mediated by Tryptophan Metabolism.Frontiers in cellular and infection microbiology · 2018Review
- LYN- and AIRE-mediated tolerance checkpoint defects synergize to trigger organ-specific autoimmunity.The Journal of clinical investigation · 2016Article
- Characterization of patients with ocular myasthenia gravis - A case series.eNeurologicalSci · 2016Article
- Extensive Citrullination Promotes Immunogenicity of HSP90 through Protein Unfolding and Exposure of Cryptic Epitopes.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Epigenetics and Primary Biliary Cirrhosis: a Comprehensive Review and Implications for Autoimmunity.Clinical reviews in allergy & immunology · 2016Review
- Epigenetics and Systemic Lupus Erythematosus: Unmet Needs.Clinical reviews in allergy & immunology · 2016Review
- CD24: from a Hematopoietic Differentiation Antigen to a Genetic Risk Factor for Multiple Autoimmune Diseases.Clinical reviews in allergy & immunology · 2016Review
- Complexity and Diversity of the Mammalian Sialome Revealed by Nidovirus Virolectins.Cell reports · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Why exactly some individuals develop autoimmune disorders remains unclear. The broadly accepted paradigm is that genetic susceptibility results in some break in immunological tolerance, may enhance the availability of autoantigens, and may enhance inflammatory responses. Some environmental insults that occur on this background of susceptibility may then contribute to autoimmunity. In this review we discuss some aspects related to inhibitory signaling and rare genetic variants, as well as additional factors that might contribute to autoimmunity including the possible role of clonal somatic mutations, the role of epigenetic events and the contribution of the intestinal microbiome. Genetic susceptibility alleles generally contribute to the loss of immunological tolerance, the increased availability of autoantigens, or an increase in inflammation. Apart from common genetic variants, rare loss-of-function genetic variants may also contribute to the pathogenesis of autoimmunity. Studies of an inhibitory signaling pathway in B cells helped identify a negative regulatory enzyme called sialic acid acetyl esterase. The study of rare genetic variants of this enzyme provides an illustrative example showing the importance of detailed functional analyses of variant alleles and the need to exclude functionally normal common or rare genetic variants from analysis. It has also become clear that pathways that are functionally impacted by either common or rare defective variants can also be more significantly compromised by gene expression changes that may result from epigenetic alterations. Another important and evolving area that has been discussed relates to the role of the intestinal microbiome in influencing helper T cell polarization and the development of 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 Socratic graph.