ReviewJournal of autoimmunity2010
Viral triggers for autoimmunity: is the 'glass of molecular mimicry' half full or half empty?
Review in Journal of autoimmunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed.
- Inhibition of pyrimidine de novo synthesis fosters Treg cells and reduces diabetes development in models of Type 1 Diabetes.Molecular metabolism · 2025Article
- Impact of Parabacteroides distasonis colonization on host microbiome, metabolome, immunity, and diabetes onset.Journal of molecular endocrinology · 2025Article
- Article
- Immunological and virological triggers of type 1 diabetes: insights and implications.Frontiers in immunology · 2023Review
- Expression of HLA and Autoimmune Pathway Genes in Liver Biopsies of Young Subjects With Autoimmune Hepatitis Type 1.Journal of pediatric gastroenterology and nutrition · 2022Article
- Incidence of Type 1 Diabetes Mellitus and Characteristics of Diabetic Ketoacidosis in Children and Adolescents during the First Two Years of the COVID-19 Pandemic in Vojvodina.Medicina (Kaunas, Lithuania) · 2022Article
- Animal Models for Autoimmune Hepatitis: Are Current Models Good Enough?Frontiers in immunology · 2022Review
- Occupational mimics of rheumatoid arthritis: hair dye-induced arthritis.Rheumatology international · 2021Review
- Chemokines as Drivers of the Autoimmune Destruction in Type 1 Diabetes: Opportunity for Therapeutic Intervention in Consideration of an Optimal Treatment Schedule.Frontiers in endocrinology · 2020Review
- Examining pathogenic concepts of autoimmune hepatitis for cues to future investigations and interventions.World journal of gastroenterology · 2019Review
- Viral Infections and Autoimmune Disease: Roles of LCMV in Delineating Mechanisms of Immune Tolerance.Viruses · 2019Review
- Viral Hormones: Expanding Dimensions in Endocrinology.Endocrinology · 2019Review
- Autoantibodies in Autoimmune Hepatitis: Can Epitopes Tell Us about the Etiology of the Disease?Frontiers in immunology · 2018Review
- Viral tRNA Mimicry from a Biocommunicative Perspective.Frontiers in microbiology · 2017Review
- TRAF3 signaling: Competitive binding and evolvability of adaptive viral molecular mimicry.Biochimica et biophysica acta · 2016Review
- Transitioning from Idiopathic to Explainable Autoimmune Hepatitis.Digestive diseases and sciences · 2015Review
- Enterovirus and type 1 diabetes: What is the matter?World journal of diabetes · 2015Review
- Inflammation and vitamin D: the infection connection.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2014Review
- Hair dyes as a risk for autoimmunity: from systemic lupus erythematosus to primary biliary cirrhosis.Auto- immunity highlights · 2013Article
- Liver immunology.Comprehensive Physiology · 2013Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
In this review we want to consider some of the requirements for autoimmune disease to develop and how this may be reproduced in animal models. Besides a genetic predisposition, environmental triggering factors seem to play a central role in the etiology of many autoimmune diseases. In theory, a structural similarity or identity between the host and an invading pathogen might cause the immune system of the host to react not only to the pathogen but also to self-components. However, in order for such a process of molecular mimicry to induce autoimmunity the mechanisms of maintaining tolerance or ignorance to the self-components need to be circumvented. Subsequently, in order to advance autoimmunity to overt autoimmune disease the frequency and avidity of autoaggressive lymphocytes has to be of sufficient magnitude. Intuitively, one would assume that tolerance might be stronger to identical structures than to structures that just share a certain degree of similarity. Self-reactive lymphocytes with high-avidity are more likely to be deleted or functionally silenced by central and/or peripheral tolerance mechanisms. Thus, perfect mimicry between identical structures might fail in inducing autoimmunity because of efficient tolerance mechanisms. In contrast, imperfect mimicry between similar but not identical structures might on one hand circumvent tolerance but on the other hand result in the generation of lymphocytes with only low- to intermediate avidity. Here we examine animal models that use the concept of molecular mimicry as a potential mechanism for inducing or accelerating autoimmunity. We focus on the RIP-LCMV model for type 1 diabetes and the novel cytochrome P450 2D6 (CYP2D6) model for autoimmune hepatitis, which use either identical or similar triggering and target antigens.
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Registered trials
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