ArticleScientific reports2017
CXCR2 deficient mice display macrophage-dependent exaggerated acute inflammatory responses.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 22 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
22 citing papers in PubMed, 31 citations in OpenAlex.
- CCR2-driven monocyte recruitment is protective against radiotherapy-induced intestinal toxicity.Mucosal immunology · 2026Article
- Cxcr2 is Required for Osteoclast Regulation, Bone Structure, and Hematological Response During Bone (Re)modeling.Calcified tissue international · 2026Article
- Inhibition of IL-27 signaling regulates chemokine levels and sustains CXCR2 receptor expression on mononuclear cells to improve disease outcomes during gram-negative neonatal sepsis.Frontiers in immunology · 2025Article
- Immunomodulatory Mechanisms of Rehmanniae Radix Praeparata-Achyranthes Root-Chinese Angelica Root Combination in Nontraumatic Osteonecrosis of the Femoral Head: A Comprehensive Network Pharmacology and Molecular Docking Study Focusing on Immunological Pathways.Mediators of inflammation · 2025Article
- Augmenting fibronectin levels in injured adult CNS promotes axon regeneration in vivo.Experimental neurology · 2024Article
- The dual-function chemokine receptor CCR2 drives migration and chemokine scavenging through distinct mechanisms.Science signaling · 2023Article
- Rabies virus uniquely reprograms the transcriptome of human monocyte-derived macrophages.Frontiers in cellular and infection microbiology · 2023Article
- Immunomodulation by radiotherapy in tumour control and normal tissue toxicity.Nature reviews. Immunology · 2022Review
- Loss ofBladder cancer (Amsterdam, Netherlands) · 2022Article
- Suppressing MDSC Recruitment to the Tumor Microenvironment by Antagonizing CXCR2 to Enhance the Efficacy of Immunotherapy.Cancers · 2021Review
- Neutrophil-specific deletion of Syk results in recruitment-independent stabilization of the barrier and a long-term improvement in cognitive function after traumatic injury to the developing brain.Neurobiology of disease · 2021Article
- Understanding the mechanisms that facilitate specificity, not redundancy, of chemokine-mediated leukocyte recruitment.Immunology · 2020Review
- The emerging role of neutrophils as modifiers of recovery after traumatic injury to the developing brain.Experimental neurology · 2019Review
- The chemokine receptor CXCR2 contributes to murine adipocyte development.Journal of leukocyte biology · 2019Article
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- Mouse Models and Tools for theFrontiers in immunology · 2019Review
- Transcription Profiling of Monocyte-Derived Macrophages InfectedFrontiers in genetics · 2019Article
- TRPM2 Exacerbates Central Nervous System Inflammation in Experimental Autoimmune Encephalomyelitis by Increasing Production of CXCL2 Chemokines.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Myeloid-derived Suppressor Cells Are Necessary for Development of Pulmonary Hypertension.American journal of respiratory cell and molecular biology · 2018Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
CXCR2 is an essential regulator of neutrophil recruitment to inflamed and damaged sites and plays prominent roles in inflammatory pathologies and cancer. It has therefore been highlighted as an important therapeutic target. However the success of the therapeutic targeting of CXCR2 is threatened by our relative lack of knowledge of its precise in vivo mode of action. Here we demonstrate that CXCR2-deficient mice display a counterintuitive transient exaggerated inflammatory response to cutaneous and peritoneal inflammatory stimuli. In both situations, this is associated with reduced expression of cytokines associated with the resolution of the inflammatory response and an increase in macrophage accumulation at inflamed sites. Analysis using neutrophil depletion strategies indicates that this is a consequence of impaired recruitment of a non-neutrophilic CXCR2 positive leukocyte population. We suggest that these cells may be myeloid derived suppressor cells. Our data therefore reveal novel and previously unanticipated roles for CXCR2 in the orchestration of the inflammatory response.
Identifiers
What OpenQuestion holds
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.