ArticlePLoS computational biology2012
A mathematical model of CR3/TLR2 crosstalk in the context of Francisella tularensis infection.
Article in PLoS computational biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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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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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- A mechanistic modelling approach of the host-microbiota interactions to investigate beneficial symbiotic resilience in the human gut.Journal of the Royal Society, Interface · 2024Article
- Stochastic dynamics of Francisella tularensis infection and replication.PLoS computational biology · 2020Article
- Complement Receptor 3-Mediated Inhibition of Inflammasome Priming by Ras GTPase-Activating Protein DuringFrontiers in immunology · 2018Article
- Mathematical Models for Immunology: Current State of the Art and Future Research Directions.Bulletin of mathematical biology · 2016Review
- Exosomal miRs in Lung Cancer: A Mathematical Model.PloS one · 2016Article
- Non-canonical Activation of Akt in Serum-Stimulated Fibroblasts, Revealed by Comparative Modeling of Pathway Dynamics.PLoS computational biology · 2015Article
- Dynamics of a Tularemia Outbreak in a Closely Monitored Free-Roaming Population of Wild House Mice.PloS one · 2015Article
- Inflammasome priming is similar for francisella species that differentially induce inflammasome activation.PloS one · 2015Article
- Lyn mitigates mouse airway remodeling by downregulating the TGF-β3 isoform in house dust mite models.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Adherence and uptake of Francisella into host cells.Virulence · 2013Review
- Fine tuning inflammation at the front door: macrophage complement receptor 3-mediates phagocytosis and immune suppression for Francisella tularensis.PLoS pathogens · 2013Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Complement Receptor 3 (CR3) and Toll-like Receptor 2 (TLR2) are pattern recognition receptors expressed on the surface of human macrophages. Although these receptors are essential components for recognition by the innate immune system, pathogen coordinated crosstalk between them can suppress the production of protective cytokines and promote infection. Recognition of the virulent Schu S4 strain of the intracellular pathogen Francisella tularensis by host macrophages involves CR3/TLR2 crosstalk. Although experimental data provide evidence that Lyn kinase and PI3K are essential components of the CR3 pathway that influences TLR2 activity, additional responsible upstream signaling components remain unknown. In this paper we construct a mathematical model of CR3 and TLR2 signaling in response to F. tularensis. After demonstrating that the model is consistent with experimental results we perform numerical simulations to evaluate the contributions that Akt and Ras-GAP make to ERK inhibition. The model confirms that phagocytosis-associated changes in the composition of the cell membrane can inhibit ERK activity and predicts that Akt and Ras-GAP synergize to inhibit ERK.
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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.