ArticleCell research2011
A MyD88-dependent IFNγR-CCR2 signaling circuit is required for mobilization of monocytes and host defense against systemic bacterial challenge.
Article in Cell research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 26 citations in OpenAlex.
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- IgM-mediated protection drives early B-cell activation and mucosal containment ofFrontiers in immunology · 2026Article
- Glucocorticoid-mediated suppression of the CCL2-CCR2 axis drives monocyte dysfunction in severe pneumonia among immunocompromised hosts.Respiratory research · 2025Article
- A distinct metabolic and epigenetic state drives trained immunity in HSC-derived macrophages from autoimmune mice.Cell stem cell · 2024Article
- Cross-Kingdom Pathogenesis ofMicroorganisms · 2024Article
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- Innate immune responses at the asymptomatic stage of influenza A viral infections of Streptococcus pneumoniae colonized and non-colonized mice.Scientific reports · 2021Article
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- Opposing effects of antibiotics and germ-free status on neuropeptide systems involved in social behaviour and pain regulation.BMC neuroscience · 2020Article
- IRAK-M Regulates Monocyte Trafficking to the Lungs in Response to Bleomycin Challenge.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
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- Sphingosine 1-Phosphate- and C-C Chemokine Receptor 2-Dependent Activation of CD4Frontiers in immunology · 2017Article
- MyD88 signaling in CD4 T cells promotes IFN-γ production and hematopoietic progenitor cell expansion in response to intracellular bacterial infection.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Review
- Route of Infection Determines the Impact of Type I Interferons on Innate Immunity to Listeria monocytogenes.PloS one · 2013Article
- MyD88-dependent recruitment of monocytes and dendritic cells required for protection from pulmonary Burkholderia mallei infection.Infection and immunity · 2012Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Monocytes are mobilized to sites of infection via interaction between the chemokine MCP-1 and its receptor, CCR2, at which point they differentiate into macrophages that mediate potent antimicrobial effects. In this study, we investigated the mechanisms by which monocytes are mobilized in response to systemic challenge with the intracellular bacterium Francisella tularensis. We found that mice deficient in MyD88, interferon-γ (IFNγ)R or CCR2 all had defects in the expansion of splenic monocyte populations upon F. tularensis challenge, and in control of F. tularensis infection. Interestingly, MyD88-deficient mice were defective in production of IFNγ, and IFNγR-deficient mice exhibited defective production of MCP-1, the ligand for CCR2. Transplantation of IFNγR-deficient bone marrow (BM) into wild-type mice further suggested that mobilization of monocytes in response to F. tularensis challenge required IFNγR expression on BM-derived cells. These studies define a critical host defense circuit wherein MyD88-dependent IFNγ production signals via IFNγR expressed on BM-derived cells, resulting in MCP-1 production and activation of CCR2-dependent mobilization of monocytes in the innate immune response to systemic F. tularensis challenge.
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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.