ArticleNature medicine2010
CX3CR1 is required for airway inflammation by promoting T helper cell survival and maintenance in inflamed lung.
Article in Nature medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 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.
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.
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Who cites it
73 citing papers in PubMed, 124 citations in OpenAlex.
- The CX3CL1-CX3CR1 axis in HIV-associated inflammation and cardiometabolic disease.American journal of physiology. Regulatory, integrative and comparative physiology · 2026Review
- CX3CR1-T280M polymorphism and end-stage renal disease development in chronic kidney disease.Scientific reports · 2026Observational
- Fractalkine (Chemokine CX3CL1) Signaling During Placentation and Placental Function.International journal of molecular sciences · 2026Review
- Alpha-toxin-elicited CXmBio · 2025Article
- RNA Sequencing Reveals Inflammatory and Metabolic Changes in the Lung and Brain After Carbon Black and Naphthalene Whole Body Inhalation Exposure in a Rodent Model of Military Burn Pit Exposures.International journal of molecular sciences · 2025Article
- Organ-specific microenvironments drive divergent T cell evolution in acute graft-versus-host disease.Science translational medicine · 2025Article
- Recent Evidence of the Role of CD4JMA journal · 2025Review
- Conserved and tissue-specific immune responses to biologic scaffold implantation.Acta biomaterialia · 2024Article
- Article
- CX3CL1 (Fractalkine)-CX3CR1 Axis in Inflammation-Induced Angiogenesis and Tumorigenesis.International journal of molecular sciences · 2024Review
- Recruitment and Maintenance of CX3CR1+CD4+ T Cells during Helminth Infection.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Leveraging genetics to investigate causal effects of immune cell phenotypes in periodontitis: a mendelian randomization study.Frontiers in genetics · 2024Article
- Conserved and tissue-specific immune responses to biologic scaffold implantation.bioRxiv : the preprint server for biology · 2023Article
- Article
- CXInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Review
- RSV pre-fusion F protein enhances the G protein antibody and anti-infectious responses.NPJ vaccines · 2022Article
- Immune phenotypes that are associated with subsequent COVID-19 severity inferred from post-recovery samples.Nature communications · 2022Article
- Immune phenotypes that predict COVID-19 severity.Research square · 2022Article
- Identification of Potential Therapeutic Target Genes in Osteoarthritis.Evidence-based complementary and alternative medicine : eCAM · 2022Article
13 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Allergic asthma is a T helper type 2 (T(H)2)-dominated disease of the lung. In people with asthma, a fraction of CD4(+) T cells express the CX3CL1 receptor, CX3CR1, and CX3CL1 expression is increased in airway smooth muscle, lung endothelium and epithelium upon allergen challenge. Here we found that untreated CX3CR1-deficient mice or wild-type (WT) mice treated with CX3CR1-blocking reagents show reduced lung disease upon allergen sensitization and challenge. Transfer of WT CD4(+) T cells into CX3CR1-deficient mice restored the cardinal features of asthma, and CX3CR1-blocking reagents prevented airway inflammation in CX3CR1-deficient recipients injected with WT T(H)2 cells. We found that CX3CR1 signaling promoted T(H)2 survival in the inflamed lungs, and injection of B cell leukemia/lymphoma-2 protein (BCl-2)-transduced CX3CR1-deficient T(H)2 cells into CX3CR1-deficient mice restored asthma. CX3CR1-induced survival was also observed for T(H)1 cells upon airway inflammation but not under homeostatic conditions or upon peripheral inflammation. Therefore, CX3CR1 and CX3CL1 may represent attractive therapeutic targets in asthma.
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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.