الفهرس 
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Abstract
Systemic lupus erythematosus (SLE) is systemic autoimmune disease, characterized by diverse multisystem involvement and the production of an array of autoantibodies. Clinical features in individual patients can be quite variable and range from mild joint and skin involvement to severe and life-threatening disease. Identification of readily available biomarkers is necessary since the clinical and paraclinical techniques to evaluate disease activity and anticipate the disease course are insufficient.
Type I IFN is the most crucial cytokine in SLE and its activation is a driver of SLE pathogenesis. Immune complexes (ICs) of autoantibodies directed against nuclear constituents in various tissues are considered a key inducer of type I IFNs in SLE. Gal-9 is a potential biomarker for the interferon signature classified as an immune checkpoint molecule and correlates with disease activity in different autoimmune diseases with regard to SLE pathogenesis. Gal-9 regulates TLR7/TLR9-signaling pathways to inhibit pDC and B cell activation.
Aim of the work: To measure the level of serum Gal-9 in SLE patients and assess its association with disease activity and disease severity.
Patients and methods: A total of 50 SLE patients and 28 controls were included in the study. Anti nuclear antibody (ANA), anti double stranded DNA antibody (anti-dsDNA), complement 3(C3), disease activity score (SLEDAI-2K), renal disease activity score (r-SLEDAI) and SLE induced organ damage (SLICC/ACR-DI) were assessed in SLE patients. Serum Gal-9 was measured in SLE patients and the healthy matching controls.
Results: The mean age of SLE patients and controls was 31.12 ± 8.68 and 31.68 ± 6.91 years respectively and the majority of studied population were females.
Serum Gal-9 level was significantly higher in SLE patients compared to healthy controls (890.14 ± 1740.39 vs. 266.85 ± 37.98; P < 0.0001; respectively). Serum Gal-9 level was significantly higher among active SLE patients compared to inactive SLE patients (1246.97 ± 2144.89 vs 307.95 ± 29.37, P<0.001; respectively). Gal-9 was significantly higher in patients with lupus nephritis in comparison to those without lupus nephritis (1377.89 ± 2273.77 vs 317.57 ± 40.36, P<0.001; respectively). Serum Gal-9 correlated significantly and positively with anti-dsDNA antibody positivity (r=0.292, p= 0.040) and negatively with serum albumin level (r= - 0.298, p = 0.06). Also; Gal-9 show significant positive correlations with SLEDAI and r SLEDAI (r=0.608, p <0.001 and r=0.610, p <0.001; respectively).
At cutoff value of 299 ng/l; serum Gal-9 can significantly differentiate SLE patients from controls (AUC 0.97; p<0.0001) with sensitivity of 88%, specificity of 75 % and accuracy of 83.3%. Also; at a cut-off value of 335 ng/l; serum Gal-9 can significantly differentiate active from inactive SLE patients (AUC 0.94; p <0.0001) at a sensitivity of 90%, specificity of 84.2%, and accuracy of 88%.
Conclusion: The serum Gal-9 levels were significantly high in SLE patients compared to healthy controls and in active SLE patients compared to those with inactive disease. Also; high serum Gal-9 levels were associated with renal affection in SLE patients.