ReviewInternational journal of molecular sciences2023
From Co-Infections to Autoimmune Disease via Hyperactivated Innate Immunity: COVID-19 Autoimmune Coagulopathies, Autoimmune Myocarditis and Multisystem Inflammatory Syndrome in Children.
Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed.
- Proteomic signals are not equal clinical phenotypes: redefining evidence standards in arbovirus-SARS-CoV-2 cross-reactivity.Frontiers in immunology · 2026Review
- Toll-like receptors in infectious myocarditis: pathogen-specific recognition, spatiotemporal dynamic regulation and clinical translation.Frontiers in cardiovascular medicine · 2026Review
- Deep insight into cytokine storm: from pathogenesis to treatment.Signal transduction and targeted therapy · 2025Review
- TLR2 Activation as a Marker of Severe COVID-19 and a Potential Therapeutic Target.Current medicinal chemistry · 2025Review
- The impact of the mRNA COVID-19 vaccine on the Th-like cytokine profile in individuals with no history of COVID-19: insights into autoimmunity targeting heat shock proteins.Frontiers in immunology · 2025Article
- Different patterns of leukocyte immune responses to infection of ancestral SARS-CoV-2 and its variants.Frontiers in cellular and infection microbiology · 2025Article
- Mechanisms underlying sex differences in autoimmunity.The Journal of clinical investigation · 2024Review
- Simultaneous occurrence of autoimmune hepatitis and autoimmune hemolytic anemia after COVID-19 infection: case report and literature review.Clinical journal of gastroenterology · 2024Review
- T-Cell Receptor Sequences Identify Combined Coxsackievirus-International journal of molecular sciences · 2024Article
- Multiple sclerosis and COVID-19: a bidirectional Mendelian randomization study.Frontiers in immunology · 2024Article
- Knowledge mapping of COVID-19 and autoimmune diseases: a visual and bibliometric analysis.Clinical and experimental medicine · 2023Article
- Impact of COVID-19 on thyroid gland functions with reference to Graves' disease: A systematic review.Journal of family medicine and primary care · 2023Review
- Health disparities in COVID-19: immune and vascular changes are linked to disease severity and persist in a high-risk population in Riverside County, California.BMC public health · 2023Article
- SARS-CoV-2 and Its Bacterial Co- or Super-Infections Synergize to Trigger COVID-19 Autoimmune Cardiopathies.International journal of molecular sciences · 2023Article
- Self-DNA driven inflammation in COVID-19 and after mRNA-based vaccination: lessons for non-COVID-19 pathologies.Frontiers in immunology · 2023Article
Corrections and comments
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neutrophilia and the production of neutrophil extracellular traps (NETs) are two of many measures of increased inflammation in severe COVID-19 that also accompany its autoimmune complications, including coagulopathies, myocarditis and multisystem inflammatory syndrome in children (MIS-C). This paper integrates currently disparate measures of innate hyperactivation in severe COVID-19 and its autoimmune complications, and relates these to SARS-CoV-2 activation of innate immunity. Aggregated data include activation of Toll-like receptors (TLRs), nucleotide-binding oligomerization domain (NOD) receptors, NOD leucine-rich repeat and pyrin-domain-containing receptors (NLRPs), retinoic acid-inducible gene I (RIG-I) and melanoma-differentiation-associated gene 5 (MDA-5). SARS-CoV-2 mainly activates the virus-associated innate receptors TLR3, TLR7, TLR8, NLRP3, RIG-1 and MDA-5. Severe COVID-19, however, is characterized by additional activation of TLR1, TLR2, TLR4, TLR5, TLR6, NOD1 and NOD2, which are primarily responsive to bacterial antigens. The innate activation patterns in autoimmune coagulopathies, myocarditis and Kawasaki disease, or MIS-C, mimic those of severe COVID-19 rather than SARS-CoV-2 alone suggesting that autoimmunity follows combined SARS-CoV-2-bacterial infections. Viral and bacterial receptors are known to synergize to produce the increased inflammation required to support autoimmune disease pathology. Additional studies demonstrate that anti-bacterial antibodies are also required to account for known autoantigen targets in COVID-19 autoimmune complications.
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What Socratic 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 Socratic graph.