ArticleImmunology and cell biology2013
Host genetic background impacts modulation of the TLR4 pathway by RON in tissue-associated macrophages.
Article in Immunology and cell biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- Modulation of host lung immunity in Pneumocystis pneumonia: a review of current concepts and future prospects for novel adjunctive immune-based therapies.Journal of immunology (Baltimore, Md. : 1950) · 2026Review
- MSP-RON signaling in liver pathobiology and as an emerging therapeutic target: a review of the current evidence.Cell communication and signaling : CCS · 2025Review
- Radiofrequency ablation plays double role in immunosuppression and activation of PBMCs in recurrent hepatocellular carcinoma.Frontiers in immunology · 2024Article
- A network map of macrophage-stimulating protein (MSP) signaling.Journal of cell communication and signaling · 2023Article
- Review
- MSP-RON Pathway: Potential Regulator of Inflammation and Innate Immunity.Frontiers in immunology · 2020Review
- TLR4, but Neither Dectin-1 nor Dectin-2, Participates in the Mollusk Hemocyanin-Induced Proinflammatory Effects in Antigen-Presenting Cells From Mammals.Frontiers in immunology · 2019Article
- The keratin 16 null phenotype is modestly impacted by genetic strain background in mice.Experimental dermatology · 2018Article
- Intrinsic Programming of Alveolar Macrophages for Protective Antifungal Innate Immunity AgainstFrontiers in immunology · 2018Article
- Recovery from an acute systemic and central LPS-inflammation challenge is affected by mouse sex and genetic background.PloS one · 2018Article
- Lactation-Based Maternal Educational Immunity Crosses MHC Class I Barriers and Can Impart Th1 Immunity to Th2-Biased Recipients.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Periodontal pathogens invade gingiva and aortic adventitia and elicit inflammasome activation in αvβ6 integrin-deficient mice.Infection and immunity · 2015Article
- Myeloid colony-stimulating factors as regulators of macrophage polarization.Frontiers in immunology · 2014Review
- Regulation of Macrophage Polarization by RON Receptor Tyrosine Kinase Signaling.Frontiers in immunology · 2014Review
- Functional consequences of the macrophage stimulating protein 689C inflammatory bowel disease risk allele.PloS one · 2013Article
- Inhibition of RON kinase potentiates anti-CTLA-4 immunotherapy to shrink breast tumors and prevent metastatic outgrowth.OncoimmunologyArticle
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Toll-like receptors (TLRs) enable metazoans to mount effective innate immune responses to microbial and viral pathogens, as well as to endogenous host-derived ligands. It is understood that genetic background of the host can influence TLR responsiveness, altering susceptibility to pathogen infection, autoimmunity and cancer. Macrophage stimulatory protein (MSP), which activates the receptor tyrosine kinase recepteur d'origine nantais (RON), promotes key macrophage functions such as motility and phagocytic activity. MSP also acts via RON to modulate signaling by TLR4, which recognizes a range of pathogen or endogenous host-derived molecules. Here, we show that RON exerts divergent control over TLR4 activity in macrophages from different mouse genetic backgrounds. RON potently modulated the TLR4 response in macrophages from M2-prone FVB mice, as compared with M1-skewed C57Bl6 mice. Moreover, global expression analysis revealed that RON suppresses the TLR4-dependent type-I interferon gene signature only in FVB macrophages. This leads to attenuated production of the potent inflammatory mediator, tumor necrosis factor-α. Eliminating RON kinase activity markedly decreased carcinogen-mediated tumorigenesis in M2/Th2-biased FVB mice. We propose that host genetic background influences RON function, thereby contributing to the variability in TLR4 responsiveness in rodents and, potentially, in humans. These findings provide novel insight into the complex interplay between genetic context and immune function.
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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.