ArticleScience signaling2010
Microbial hijacking of complement-toll-like receptor crosstalk.
Article in Science signaling, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 135 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.
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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
135 citing papers in PubMed, 217 citations in OpenAlex.
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- Salivary antibody responses toJournal of advanced periodontology & implant dentistry · 2026Article
- Supramolecular strategy for compartment pathogen clearance and immuno-metabolic homeostasis to treat periodontitis.Nature communications · 2026Article
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- Porphyromonas gingivalis Suppresses Interferon-Gamma Signaling in Macrophages Through a Contact-Dependent, Gingipain-Mediated Mechanism.MicrobiologyOpen · 2026Article
- Macrophage activation and invasion byJournal of oral microbiology · 2026Article
- Anaerobe-associated microbial shifts at infection onset in diabetes-related foot ulcers revealed by longitudinal metagenomics.Frontiers in cellular and infection microbiology · 2026Article
- The survival status ofJournal of oral microbiology · 2026Review
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- Effects of Oral Appliance Therapy with a Mouth Shield in Periodontitis Patients Who Snore: A Split-Mouth Randomized Controlled Trial.Dentistry journal · 2025Article
- From Childhood Woes to Adult Blues: Unmasking the Role of Early Traumas, P2X7 Receptor, and Neuroinflammation in Anxiety and Depression.International journal of molecular sciences · 2025Review
- CTLA-4 and targeted immunotherapy-a key link in the systemic influence of periodontitis: a mini review.Frontiers in dental medicine · 2025Review
- CD47 and thrombospondin-1 contribute to immune evasion byProceedings of the National Academy of Sciences of the United States of America · 2024Article
- The complement system: A key player in the host response to infections.European journal of immunology · 2024Review
- The Effect of Acute High-Altitude Exposure on Oral Pathogenic Bacteria and Salivary Oxi-Inflammatory Markers.Journal of clinical medicine · 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
- Arginine-specific gingipains (RgpA/RgpB) knockdown modulates neutrophil machinery.Journal of oral microbiology · 2024Article
- An Overview of Chronic Kidney Disease Pathophysiology: The Impact of Gut Dysbiosis and Oral Disease.Biomedicines · 2023Review
75 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
10 authors at 2 institutions in 1 country.
Funding
Abstract
Crosstalk between complement and Toll-like receptors (TLRs) coordinates innate immunity. We report a previously unknown immune subversion mechanism involving microbial exploitation of communication between complement and TLRs. Porphyromonas gingivalis, a major oral and systemic pathogen with complement C5 convertase-like activity, synergizes with C5a (fragment of complement protein C5) to increase cyclic adenosine monophosphate (cAMP) concentrations, resulting in suppression of macrophage immune function and enhanced pathogen survival in vitro and in vivo. This synergy required TLR2 signaling, a pertussis toxin- and thapsigargin-sensitive C5a receptor pathway, with protein kinase A and glycogen synthase kinase-3beta as downstream effectors. Antagonistic blockade of the C5a receptor abrogated this evasive strategy and may thus have important therapeutic implications for periodontitis and atherosclerosis, diseases in which P. gingivalis is implicated. This first demonstration of complement-TLR crosstalk for immunosuppressive cAMP signaling indicates that pathogens may not simply undermine complement or TLRs (or both) as separate entities, but may also exploit their crosstalk pathways.
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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.