Role of Fractalkine/CX3CL1 and Its Receptor in the Pathogenesis of Inflammatory and Malignant Diseases with Emphasis on B Cell Malignancies

Table 1

Role of CX3CL1/CX3CR1 axis in inflammation and neurodegenerative diseases.

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