An Overview of the Role of Chemokine CX3CL1 (Fractalkine) and CX3C
Chemokine Receptor 1 in Systemic Sclerosis
Abstract
Systemic sclerosis (SSc) is an autoimmune rheumatic disorder
distinguished with fibrosis and vascular injury and structural
alteration, coexisting with Reynaud’s phenomenon. The crosstalk between
activated fibroblasts, immune effectors, and endothelial cells are the
primary culprits in disease process. Fractalkine (FKN) or CX3CL1 is an
unremarkable membrane-bound soluble chemokine and an adhesion molecule
expressed on pro-inflammatory cytokine. In this systematic review, FKN
and its receptor’s (CX3CR1) role in mediating inflammatory processes
focusing on the pathogenesis of SSc is investigated. FKN is one of the
most influential molecules which monitors the trafficking of
inflammatory cells through the endothelium and has been observed to have
pronounced expression in inflammation. The correlation between increased
CX3CL1 levels in SSc and interstitial lung disease was established, and
it was noted that CX3CL1 is predominantly co-localized with infiltrating
mononuclear cells and epithelia within the lungs. The interstitial lung
disease prediction and its progression may be available through
augmented concentrations in SSc patients. Conclusively, Emerging
evidence claims that FKN could be expressed in numerous tissues, taking
part in the CX3CR1 positive cell accumulation at sites of inflammation
and, as a result, involved in countless rheumatic diseases such as
rheumatoid arthritis, Systemic lupus erythematosus, and scleroderma.
Besides, it may play a prominent part in the SSc pathogenesis, involving
vascular injury and tissue inflammation. Its estimation could be used as
a serological marker for the recognition and follow-up of skin and
pulmonary complications.