ReviewDiabetologia2015
Lessons from the mouse: potential contribution of bystander lymphocyte activation by viruses to human type 1 diabetes.
Review in Diabetologia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 46 citations in OpenAlex.
- Rotavirus Infection as a Contributor to Early-Onset Type 1 Diabetes: Review and Recommendations.Viruses · 2026Review
- Review
- Beyond inflammation: the multifaceted therapeutic potential of targeting the CXCL8-CXCR1/2 axis in type 1 diabetes.Frontiers in immunology · 2025Review
- Mechanisms governing bystander activation of T cells.Frontiers in immunology · 2024Review
- Covid-19 infection in children and adolescents and its association with type 1 diabetes mellitus (T1d) presentation and management.Endocrine · 2023Review
- Steady-state memory-phenotype conventional CD4Experimental & molecular medicine · 2023Article
- Molecular Mimicry Analyses Unveiled the Human Herpes Simplex and Poxvirus Epitopes as Possible Candidates to Incite Autoimmunity.Pathogens (Basel, Switzerland) · 2022Article
- Rotavirus vaccination is not associated with incident celiac disease or autoimmune thyroid disease in a national cohort of privately insured children.Scientific reports · 2022Article
- Emerging role of bystander T cell activation in autoimmune diseases.BMB reports · 2022Review
- Viruses and Type 1 Diabetes: From Enteroviruses to the Virome.Microorganisms · 2021Review
- Enteric viruses evoke broad host immune responses resembling those elicited by the bacterial microbiome.Cell host & microbe · 2021Article
- Deficiency of the innate immune adaptor STING promotes autoreactive T cell expansion in NOD mice.Diabetologia · 2021Article
- Rotavirus and Type 1 Diabetes-Is There a Connection? A Synthesis of the Evidence.The Journal of infectious diseases · 2020Review
- TLR9 Sensing of Self-DNA Controls Cell-Mediated Immunity to Listeria Infection via Rapid Conversion of Conventional CD4Cell reports · 2020Article
- The activation of bystander CD8Experimental & molecular medicine · 2019Review
- Viruses and Autoimmunity: A Review on the Potential Interaction and Molecular Mechanisms.Viruses · 2019Review
- Distinct Inflammatory Changes of the Pancreas of Slowly Progressive Insulin-dependent (Type 1) Diabetes.Pancreas · 2018Article
- MHC class I expression in intestinal cells is reduced by rotavirus infection and increased in bystander cells lacking rotavirus antigen.Scientific reports · 2018Article
- Autoreactive T cells in type 1 diabetes.The Journal of clinical investigation · 2017Review
- Rotavirus acceleration of type 1 diabetes in non-obese diabetic mice depends on type I interferon signalling.Scientific reports · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Viruses are considered to be potential key modulators of type 1 diabetes mellitus, with several possible mechanisms proposed for their modes of action. Here we discuss the evidence for virus involvement, including pancreatic infection and the induction of T cell-mediated molecular mimicry. A particular focus of this review is the further possibility that virus infection triggers bystander activation of pre-existing autoreactive lymphocytes. In this scenario, the virus triggers dendritic cell maturation and proinflammatory cytokine secretion by engaging pattern recognition receptors. These proinflammatory cytokines provoke bystander autoreactive lymphocyte activation in the presence of cognate autoantigen, which leads to enhanced beta cell destruction. Importantly, this mechanism does not necessarily involve pancreatic virus infection, and its virally non-specific nature suggests that it might represent a means commonly employed by multiple viruses. The ability of viruses specifically associated with type 1 diabetes, including group B coxsackievirus, rotavirus and influenza A virus, to induce these responses is also examined. The elucidation of a mechanism shared amongst several viruses for accelerating progression to type 1 diabetes would facilitate the identification of important targets for disease intervention.
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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.