ArticleThe Journal of experimental medicine2014
CX₃CL1 (fractalkine) and its receptor CX₃CR1 regulate atopic dermatitis by controlling effector T cell retention in inflamed skin.
Article in The Journal of experimental medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 65 citations in OpenAlex.
- Chemokine ligand-receptor interactions as potential therapeutic targets for atopic dermatitis: from basic to clinical research.Frontiers in allergy · 2026Review
- Recruitment and Maintenance of CX3CR1+CD4+ T Cells during Helminth Infection.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- The menstrual cycle regulates migratory CD4 T-cell surveillance in the female reproductive tract via CCR5 signaling.Mucosal immunology · 2024Article
- Loss of epidermal glucocorticoid receptor protects against whole body metabolic dysfunction upon chronic corticosterone treatment.Molecular metabolism · 2023Article
- Single-cell RNA sequencing reveals the local cell landscape in mouse epididymal initial segment during aging.Immunity & ageing : I & A · 2023Article
- Exploring Mast Cell-CD8 T Cell Interactions in Inflammatory Skin Diseases.International journal of molecular sciences · 2023Review
- CX3CR1 deficiency exacerbates immune-mediated hepatitis by increasing NF-κB-mediated cytokine production in macrophage and T cell.Experimental biology and medicine (Maywood, N.J.) · 2023Article
- Innate Immune Responses by Respiratory Viruses, Including Rhinovirus, During Asthma Exacerbation.Frontiers in immunology · 2022Review
- Review
- Cytokine changes during immune-related adverse events and corticosteroid treatment in melanoma patients receiving immune checkpoint inhibitors.Cancer immunology, immunotherapy : CII · 2021Article
- Ligand-competent fractalkine receptor is expressed on exosomes.Biochemistry and biophysics reports · 2021Article
- CX3CR1 Deficiency Attenuates DNFB-Induced Contact Hypersensitivity Through Skewed Polarization Towards M2 Phenotype in Macrophages.International journal of molecular sciences · 2020Article
- CXCells · 2019Article
- Indispensable Role of CXFrontiers in immunology · 2019Article
- Regional Distribution of CNS Antigens Differentially Determines T-Cell Mediated Neuroinflammation in a CX3CR1-Dependent Manner.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Intracapillary immune complexes recruit and activate slan-expressing CD16+ monocytes in human lupus nephritis.JCI insight · 2018Article
- Identifying a Novel Role for Fractalkine (CX3CL1) in Memory CD8Frontiers in immunology · 2018Article
- Therapeutic effects of orally administered CJLP55 for atopic dermatitis via the regulation of immune response.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2017Article
- CD4Immunology · 2017Review
- Bacterial and Viral Infections in Atopic Dermatitis: a Comprehensive Review.Clinical reviews in allergy & immunology · 2016Review
Corrections and comments
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Authors and funding
18 authors at 9 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atopic dermatitis (AD) is a chronic allergic dermatosis characterized by epidermal thickening and dermal inflammatory infiltrates with a dominant Th2 profile during the acute phase, whereas a Th1 profile is characteristic of the chronic stage. Among chemokines and chemokine receptors associated with inflammation, increased levels of CX3CL1 (fractalkine) and its unique receptor, CX3CR1, have been observed in human AD. We have thus investigated their role and mechanism of action in experimental models of AD and psoriasis. AD pathology and immune responses, but not psoriasis, were profoundly decreased in CX3CR1-deficient mice and upon blocking CX3CL1-CX3CR1 interactions in wild-type mice. CX3CR1 deficiency affected neither antigen presentation nor T cell proliferation in vivo upon skin sensitization, but CX3CR1 expression by both Th2 and Th1 cells was required to induce AD. Surprisingly, unlike in allergic asthma, where CX3CL1 and CX3CR1 regulate the pathology by controlling effector CD4(+) T cell survival within inflamed tissues, adoptive transfer experiments established CX3CR1 as a key regulator of CD4(+) T cell retention in inflamed skin, indicating a new function for this chemokine receptor. Therefore, although CX3CR1 and CX3CL1 act through distinct mechanisms in different pathologies, our results further indicate their interest as promising therapeutic targets in allergic diseases.
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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.