ReviewImmunological reviews2016
More than complementing Tolls: complement-Toll-like receptor synergy and crosstalk in innate immunity and inflammation.
Review in Immunological reviews, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 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
73 citing papers in PubMed.
- Does C1 esterase inhibitor play a role in post COVID-19 neurological symptoms? A randomized, double-blind, placebo-controlled, crossover, proof-of-concept study.Frontiers in neurology · 2025Trial
- Phase IIa clinical trial of complement C3 inhibitor AMY-101 in adults with periodontal inflammation.The Journal of clinical investigation · 2021Trial
- High Glucose Induces Biomolecular Dysregulation in Primary Human Corneal Epithelial Cells: Potential Biomarkers of Hyperglycemia-Driven Corneal Impairment.International journal of molecular sciences · 2026Article
- Review
- Endothelial cell-secreted SPARC suppresses astrocytic CD59 expression and promotes astrocytopathy in a mouse model of neuromyelitis optica spectrum disorders.Nature communications · 2026Article
- The role of the complement system in gastrointestinal-related diseases.Frontiers in immunology · 2026Review
- Intracellular C3 regulates the immune response to infection via NF-κB signaling.Cellular and molecular life sciences : CMLS · 2025Article
- Complement factor D (adipsin) mediates pressure-pain hypersensitivity post destabilization of medial meniscus injury.Arthritis research & therapy · 2025Article
- Age-related inflammatory changes and perineuronal net dynamics: implications for aging.Journal of neuroinflammation · 2025Article
- Lactobacilli-Derived Microbe-Associated Molecular Patterns (MAMPs) in Host Immune Modulation.Biomolecules · 2025Review
- Article
- Age-related inflammatory changes and perineuronal net dynamics: implications for neurodegenerative disorders.bioRxiv : the preprint server for biology · 2025Article
- The trapping of live neutrophils by macrophages during infection.Cell death & disease · 2025Article
- Article
- Exploring Potential Complement Modulation Strategies for Ischemia-Reperfusion Injury in Kidney Transplantation.Antioxidants (Basel, Switzerland) · 2025Review
- Neutrophil diversity and function in health and disease.Signal transduction and targeted therapy · 2024Review
- Article
- Elucidating allergic reaction mechanisms in response to SARS-CoV-2 mRNA vaccination in adults.Allergy · 2024Article
- TLR2 and TLR4 Are Expressed in Epiretinal Membranes: Possible Links with Vitreous Levels of Complement Fragments and DAMP-Related Proteins.International journal of molecular sciences · 2024Article
- Cell-intrinsic C5a synergizes with Dectin-1 in macrophages to mediate fungal killing.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
13 more citing papers are in PubMed but not listed here.
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.
Funding
Abstract
Complement and Toll-like receptors (TLRs) play key roles in the host immune response and are swiftly activated by infection or other types of immunological stress. This review focuses on the capacity of complement and TLRs to engage in signaling crosstalk, ostensibly to coordinate immune and inflammatory responses through synergistic or antagonistic (regulatory) interactions. However, overactivation or dysregulation of either system may lead-often synergistically-to exaggerated inflammation and host tissue injury. Intriguingly, moreover, certain pathogens can manipulate complement-TLR crosstalk pathways in ways that undermine host immunity and favor their persistence. In the setting of polymicrobial inflammatory disease, subversion of complement-TLR crosstalk by keystone pathogens can promote dysbiosis. Knowledge of the molecular mechanisms underlying complement-TLR crosstalk pathways can, therefore, be used productively for tailored therapeutic approaches, such as, to enhance host immunity, mitigate destructive inflammation, or counteract microbial subversion of the host response.
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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.