CX3C Chemokines

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    Immunology Background

    Available Resources for CX3C Chemokines Research

    Creative BioMart is your premier destination for all your research requirements concerning CX3C chemokines. Our carefully curated products and tailored services are crafted to guide your exploration into the world of CX3C chemokines and their vital roles in diverse physiological processes.

    • Explore our product range to discover high-quality recombinant proteins, protein pre-coupled magnetic beads, cell and tissue lysates, and more.
    • Moreover, delve into our extensive pool of resources on CX3C chemokines, encompassing critical subjects like involved pathways, protein functions, interacting proteins, pertinent articles, and areas of ongoing research.

    Our Featured Products

    Cat.# Product name Species Source (Host) Tag
    CX3CL1-86H Recombinant Human CX3CL1 protein, His-tagged Human HEK293 His
    CX3CL1-11712H Recombinant Human CX3CL1, GST-tagged Human E.coli GST
    CX3CL1-4319B Recombinant Bovine CX3CL1 Protein Bovine Yeast N/A

    About CX3C Chemokines

    CX3C chemokines, also known as fractalkines or CX3CL chemokines, are a distinct subgroup of chemokines characterized by the presence of a unique CX3C motif. They are named after the cysteine residues separated by three amino acids (X3C) near their amino terminus. The sole member of this chemokine family is CX3CL1, also referred to as fractalkine.

    CX3CL1 is a transmembrane chemokine, meaning it can exist in both membrane-bound and soluble forms. It is expressed by various cell types, including endothelial cells, neurons, epithelial cells, and immune cells such as monocytes and macrophages. CX3CL1 interacts with its receptor, CX3CR1, which is predominantly expressed on immune cells, particularly monocytes, macrophages, and natural killer (NK) cells.

    CX3CL1 and CX3CR1 have unique features that distinguish them from other chemokines and chemokine receptors. Unlike most chemokines, CX3CL1 is a transmembrane protein with a chemokine domain located on the extracellular portion. The soluble form of CX3CL1 can be generated through proteolytic cleavage at the cell surface. CX3CR1, on the other hand, belongs to the family of G protein-coupled receptors (GPCRs) and can initiate intracellular signaling upon ligand binding.

    Intracellular signaling in endothelial cells in the induction of angiogenesis by CX3CL1.Fig.3 Intracellular signaling in endothelial cells in the induction of angiogenesis by CX3CL1. Activation of CX3CR1 causes signal transduction in endothelial cells, which causes angiogenesis. The most important activated pathways in this process are ERK MAPK and PI3K → Akt/PKB. Activation of ERK MAPK causes migration, proliferation and tube formation of endothelial cells.(Korbecki J, et al., 2022)

    Research on CX3C Chemokines

    Research on CX3C chemokines, particularly CX3CL1 and its receptor CX3CR1, has provided valuable insights into their roles in various physiological and pathological processes. Here are some key areas of research on CX3C chemokines:

    • Immune Cell Trafficking: CX3CL1 and CX3CR1 are involved in the recruitment and migration of immune cells. Studies have investigated their role in the selective recruitment of CX3CR1-expressing monocytes, macrophages, and NK cells to sites of inflammation or tissue damage. This research has provided insights into the mechanisms of immune cell trafficking and the regulation of immune responses.
    • Neuroinflammation and Neurodegenerative Disorders: CX3CL1 and CX3CR1 are expressed in the central nervous system (CNS) and play a role in neuroinflammation and neurodegenerative disorders. Research has shown that dysregulation of the CX3CL1-CX3CR1 axis is associated with neuroinflammatory conditions such as multiple sclerosis, Alzheimer's disease, Parkinson's disease, and stroke. Understanding the interactions between CX3CL1-expressing neurons and CX3CR1-expressing microglia has provided insights into the pathogenesis of these disorders and potential therapeutic targets.
    • Atherosclerosis and Cardiovascular Diseases: CX3CL1 and CX3CR1 are implicated in the development and progression of atherosclerosis, a chronic inflammatory disease of blood vessels. Research has shown that CX3CR1-expressing monocytes and macrophages play a role in the formation of atherosclerotic plaques. Inhibition of the CX3CL1-CX3CR1 axis has been investigated as a potential therapeutic strategy to reduce atherosclerosis and cardiovascular risk.
    • Cancer and Metastasis: The CX3CL1-CX3CR1 axis has been implicated in cancer progression and metastasis. Research has shown that CX3CL1 expression in tumor cells and CX3CR1 expression in immune cells can influence tumor growth, invasion, and metastasis. The interaction between CX3CL1-expressing cancer cells and CX3CR1-expressing immune cells in the tumor microenvironment has been a subject of investigation to understand the mechanisms underlying cancer progression and develop novel therapeutic approaches.
    • Therapeutic Targeting: Given the involvement of CX3CL1 and CX3CR1 in various diseases, targeting this chemokine-receptor axis has emerged as a potential therapeutic strategy. Researchers have explored the development of CX3CR1 antagonists, monoclonal antibodies against CX3CL1, and strategies to modulate CX3CR1 signaling to regulate immune responses, reduce inflammation, and potentially treat diseases such as neuroinflammatory disorders and atherosclerosis.

    Overall, research on CX3C chemokines, particularly CX3CL1 and CX3CR1, has provided valuable insights into their roles in immune cell trafficking, inflammation, and disease pathogenesis. Understanding the complex interactions between CX3CL1 and CX3CR1 in various disease contexts may lead to the development of targeted therapies for a range of conditions, including neuroinflammatory disorders, cardiovascular diseases, and cancer.

    Table 1 Role of CX3CL1/CX3CR1 axis in inflammation and neurodegenerative diseases. (Ferretti E, et al., 2024)

    Allergic asthma and rhinitis CX3CL1 increases recruitment of CX3CR1+ CD4+ T cells in the airways
    Rheumatoid arthritis CX3CL1 contributes to the accumulation in the synovium of T cells, macrophages, and dendritic cells expressing CX3CR1
    Atherosclerotic disease (i) Membrane-bound CX3CL1 promotes cell to cell interactions
    (ii) Soluble CX3CL1 directs migration of CX3CR1+ monocytes from the blood to the vessel wall
    Renal diseases CX3CL1 supports recruitment and retention of CX3CR1+ leukocytes infiltrating the kidney
    Chronic liver disease (i) CX3CL1 facilitates recruitment and adhesion of CX3CR1+ inflammatory cells to the liver
    (ii) CX3CL1 supports paracrine stimulation of hepatic stellate cells expressing CX3CR1
    Age-related macular degeneration Dysfunction in CX3CL1/CX3CR1 signaling promotes accumulation of inflammatory macrophages and microglia cells
    Crohn's disease CX3CL1 sustains homeostasis of macrophages of lamina propria expressing CX3CR1
    Alzheimer's disease (i) CX3CR1 deficiency enhances β-amyloid deposition and microglia activation
    (ii) In other models CX3CR1 depletion results in a reduction of Aβ-deposition
    Parkinson's disease (i) Soluble CX3CL1 exhibits neuroprotective properties decreasing microglial activation and proinflammatory cytokine release
    (ii) Membrane-bound CX3CL1 is not neuroprotective but mediates proinflammatory functions
    HIV infection (i) Soluble CX3CL1 inhibits apoptosis of hippocampal neurons induced by neurotoxic viral proteins
    (ii) CX3CL1 is involved in neuronal damage through its activity on microglia that secrete proinflammatory cytokines

    Table 2 Role of CX3CL1/CX3CR1 axis in cancer. (Ferretti E, et al., 2024)

    Gliomas CX3CL1 negatively regulates glioma cell invasiveness by promoting aggregation of CX3CR1+ tumor cells
    Neuroblastoma (NB) (i) Soluble CX3CL1 stimulates CX3CR1+ NB cells to transmigrate through CX3CR1+/CX3CL1+ human bone-marrow endothelium
    (ii) Deletion of CX3CL1 gene into NB cell lines induces an antitumor immune response mediated by NK cells and T lymphocytes
    Prostate cancer Soluble CX3CL1 attracts CX3CR1+ prostate cancer cells to the bone marrow and guides their preferential migration towards human osteoblasts
    Pancreatic ductal adenocarcinoma (PDAC) CX3CR1 mediates migration of PDAC cells to CX3CL1 constitutively expressed by neural cells
    Epithelial ovarian carcinoma (EOC) CX3CL1/CX3CR1 axis facilitates cell migration and cell adhesion between EOC cells and peritoneal mesothelial cells
    Breast cancer (i) CX3CR1 contributes to tumor metastasis to skeleton and brain where bone stromal cells and neurons release soluble CX3CL1
    (ii) CX3CL1 induces both innate and adaptive immunity and correlates with good prognosis
    Colorectal cancer Soluble CX3CL1, produced by colon cancer cells, attracts cytotoxic effector T lymphocytes and NK cells showing antitumor effects
    Hepatocellular carcinoma CX3CL1/CX3CR1 axis elicits tumor-specific cytotoxic T cell response and correlates with good prognosis
    Gastric adenocarcinoma CX3CL1 promotes both innate and adaptive immunities
    B-chronic lymphocytic leukemia (B-CLL) CX3CL1/CX3CR1 axis, coexpressed on B-CLL cells, is involved in the interaction between leukemic cells and tumor microenvironment
    B cell lymphomas CX3CL1/CX3CR1 axis, coexpressed on lymphoma cells, may be involved in the interaction between lymphoma cells and tumor microenvironment

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    Related References

    1. Kim KW, Vallon-Eberhard A, Zigmond E, et al. In vivo structure/function and expression analysis of the CX3C chemokine fractalkine. Blood. 2011;118(22):e156-e167.
    2. Stievano L, Piovan E, Amadori A. C and CX3C chemokines: cell sources and physiopathological implications. Crit Rev Immunol. 2004;24(3):205-228.
    3. Ferretti E, Pistoia V, Corcione A. Role of fractalkine/CX3CL1 and its receptor in the pathogenesis of inflammatory and malignant diseases with emphasis on B cell malignancies. Mediators Inflamm. 2014;2014:480941.
    4. Korbecki J, Simińska D, Kojder K, et al. Fractalkine/CX3CL1 in Neoplastic Processes. Int J Mol Sci. 2020;21(10):3723. Published 2020 May 25.