Abstract
Background/Objectives: Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by fluctuating disease activity and multi-organ involvement. The identification of reliable biomarkers that accurately reflect disease activity remains a significant clinical challenge, particularly in predicting disease flares. Chemokines are key mediators of immune cell recruitment and inflammation, making them promising candidates for disease activity monitoring. Therefore, we evaluated serum concentrations of CCL2, CCL4, CCL5, CXCL8, and CXCL10 and examined their associations with disease activity and clinical manifestations in patients with SLE. Patients and Methods: A total of 52 patients with SLE were enrolled in the study, of whom 15 (28.8%) had active disease (SLE Disease Activity Index [SLEDAI] ≥ 5) and 37 (71.2%) were in remission (SLEDAI < 5). An additional group of 12 age- and sex-matched healthy individuals without a family history of autoimmune diseases served as controls. All SLE patients fulfilled the 2019 EULAR/ACR classification criteria. Serum levels of the selected chemokines were measured in all participants using the Luminex Human Premixed Multi-Analyte Discovery Assay. Results: Serum concentrations of CCL2 and CCL4 did not differ between SLE patients and healthy controls, nor between active and inactive disease subgroups (p > 0.05, for all). In contrast, CCL5 levels were 34.30% higher in patients with SLE compared with controls (p = 0.013), with the strongest increase observed in the inactive disease subgroup as compared to controls (by 40.29%, p = 0.021). CXCL8 levels were markedly elevated in patients with active SLE relative to those in remission (by 123.30%, p = 0.011) and to healthy individuals (by 183.96%, p = 0.049). CXCL10 levels were higher in both active and inactive SLE groups compared with controls (increase of 180.80%, p < 0.001 and increase of 100.80%, p = 0.018, respectively). No differences in chemokine levels were detected between patients with renal flares and those with non-renal flares, nor among patients in remission with and without a history of lupus nephritis (p > 0.05, for all). CXCL8 and CXCL10 correlated positively with disease activity scores, inflammatory markers, and several immune parameters, indicating their relevance to ongoing inflammatory processes (p < 0.05, for all). CCL5 was associated with complement components C3 (r(S) = 0.36, p = 0.008) and C4 (r(S) = 0.38, p = 0.006), while CXCL10 showed negative correlations with white blood cell (r(S) = -0.34, p = 0.013), lymphocyte counts (r(S) = -0.36, p = 0.008) and neutrophils (r(S) = -0.32, p = 0.019). In the longitudinal follow-up of patients in remission (median follow-up time of 5.5 years), baseline chemokine levels did not predict subsequent disease flares among SLE patients who were inactive as the study baseline (p > 0.05, for all). Conclusions: In our study, serum levels of CXCL8 and CXCL10 reflect disease activity and systemic inflammation in SLE, supporting their potential value as biomarkers for monitoring ongoing immune activation. Baseline concentrations of the examined chemokines did not predict future disease flares, indicating their limited utility in this context.