Fractalkine/CX3CR1: why a single chemokine-receptor duo bears a major and unique therapeutic potential
Abstract
Importance of the field Fractalkine, also known as CX3CL1, is the unique member of the fourth class of chemokines and mediates both chemotaxis and adhesion of inflammatory cells via its highly selective receptor CX3CR1. Fractalkine mediates inflammatory responses and pain sensation and is involved in the pathogenesis and progression of numerous inflammatory disorders and malignancies. Areas covered in this review We performed a Medline/PubMed search to detect all published studies that explored the role of fractalkine and CX3CR1 and the possibilities of therapeutic intervention in the fractalkine/CX3CR1 axis in a wide range of clinical disorders, using CX3CR1 blocking antibodies, different fractalkine antagonists, CX3CR1 depletion or transfection of fractalkine expression vectors. What the reader will gain This review summarizes the role of fractalkine and its receptor CX3CR1 in various diseases, focusing on their high potential as novel therapeutic targets, with special emphasis on pancreatic diseases. Take home message The reviewed studies provide promising results demonstrating fractalkine and CX3CR1 as potential target molecules for future therapeutics that may attenuate pain, inflammation and furthermore serve as an anti-cancer therapy. However, to date, no therapeutics targeting fractalkine or CX3CR1 are in clinical use.
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CX3CR1 and its ligand fractalkine have been implicated in recruitment of mononuclear phagocytes to sites of inflammation and injury and play roles in the pathogenesis of several inflammatory conditions including atherosclerosis, neuropathic pain, and asthma.
“CX3CR1 and its chemokine ligand fractalkine (CX3CL1) have been implicated in the recruitment of mononuclear phagocytes to sites of inflammation and injury (7, 10, 11) and play roles in the pathogenesis of several inflammatory conditions, including atherosclerosis (12, 13), neuropathic pain (14), and asthma (15).”
From Heterozygous CX3CR1 Deficiency in Microglia Restores Neuronal β-Amyloid Clearance Pathways and Slows Progression of Alzheimer's Like-Disease in PS1-APP Mice (2019) · cites this paper as [11]
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References 97 · Cited by 116
- Authors
- D'Haese, J. G., Demir, I. E., Friess, H., & Ceyhan, G. O.
- Affiliations
- TUM Klinikum (DE)
- ORCID
- Friess, Helmut
- Venue
- Expert Opinion on Therapeutic Targets
- Publisher
- Informa UK Limited
- Published
- 2010-01-08
- Volume
- 14
- Issue
- 2
- Pages
- 207-219
- ISSN
- 1472-8222 (ISSN-L)
- 1744-7631
- OpenAlex
- W1975662731
- Cited by
- 116
- References
- 97
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 5 · 2023: 7 · 2022: 9 · 2021: 7 · 2020: 4 · 2019: 4 · 2018: 6 · 2017: 8 · 2016: 7 · 2015: 6 · 2014: 8 · 2013: 13 · 2012: 11
- FWCI
- 1.42
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Expert Opinion on Therapeutic Targets (publishedVersion)
- PubMed (publishedVersion)
- mediaTUM – the media and publications repository of the Technical University Munich (Technical University Munich) (submittedVersion)
- Topics
- Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
- Keywords
- fractalkine, CX3CR1, inflammatory diseases, pain, cancer therapy, pancreatic diseases, therapeutic target
- MeSH terms
- Animals, Humans, Inflammation, Neoplasms, Pain, Pancreatic Diseases, Chemokine CX3CL1
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