Background Systemic lupus erythematosus (SLE) is a systemic autoimmune disease with unknown etiology, characterized by the hyperproduction of autoantibodies to various components of the cell nucleus and the resulting immune-inflammatory damage to tissues. Current trends of personalization therapy require the search for new serum markers, the production of which reflects aberrant activation of the immune system with further formation of autoimmunity. These are cytokines, chemokines and their receptors. Our aim was to determine the levels of interleukin (IL)-1b and soluble IL-2 receptor (sIL-2R) in patients with SLE, to evaluate their association with clinical and laboratory disease manifestations.
Methods The study included 26 patients (21 women, 5 men) with a diagnosis of SLE meeting the criteria of SLICC 2012 and EULAR/ACR 2019. The mean age of the patients was 33±11 years and the median disease duration was 14 [4;144] months. Examination of patients included standard laboratory and instrumental diagnostics. Disease activity was assessed using the SLEDAI-2K index. Serum levels of IL-1b and sIL-2R were determined by enzyme immunoassay (Invitrogen, Australia).
Results In the study cohort median IL-1b and sIL-2R levels were 3,3 [2,5;4,6] ng/mL and 0,0065 [0,005;0,008] pg/mL, respectively. Only negative correlation of IL-1b level with glomerular filtration rate was found (R=-0,48, p<0,01). sIL-2R level was associated with SLEDAI-2K (R=0,53, p<0,005), anti-dsDNA (R=0,55, p<0,003), C3 (R=-0,56, p<0,003) and ferritin level (R=0,47, p<0,05), CRP (R=0,45, p<0,002), urinary casts (R=0,46, p<0,01), leukocyturia (R=0,42, p<0,03). There were no statistically significant differences in the concentrations of both studied immunological markers between patients with lupus nephritis (LN) (n=18) and without LN (n=8).
Conclusions The concentration of sIL-2R correlates with laboratory indicators of SLE, SLEDAI-2K and urine sediments, suggesting its promising potential for SLE activity evaluation. In turn, IL-1b levels may reflect renal function, which requires further study in a larger cohort of patients with SLE.
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