1. Increased serum IL-36α and IL-36γ levels in patients with systemic lupus erythematosus: Association with disease activity and arthritis
- Author
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Fan-qin Zeng, Yanfang Han, Shao-zhen Mai, Xiao-ying Xie, Min Xu, Chijun Li, Qing Guo, and Hui Xiong
- Subjects
Adult ,Male ,0301 basic medicine ,Adolescent ,medicine.medical_treatment ,Immunology ,Arthritis ,Severity of Illness Index ,Disease activity ,Young Adult ,03 medical and health sciences ,0302 clinical medicine ,medicine ,Humans ,Lupus Erythematosus, Systemic ,Immunology and Allergy ,In patient ,skin and connective tissue diseases ,Aged ,Pharmacology ,business.industry ,Complement C3 ,Receptors, Interleukin ,Middle Aged ,medicine.disease ,Reverse transcription polymerase chain reaction ,030104 developmental biology ,Cytokine ,Gene Expression Regulation ,Disease Progression ,Female ,Cytokine mrna ,business ,Biomarkers ,Interleukin-1 ,030215 immunology - Abstract
IL-36 cytokines (IL-36Ra, IL-36α, IL-36β and IL-36γ) belong to the IL-1 family and have been linked to several autoimmune diseases. However, little is known about the relationships between systemic lupus erythematosus (SLE) and IL-36 cytokines. In this study, serum IL-36 cytokine levels were determined by enzyme-linked immunosorbent assay (ELISA), and their associations with SLE-related parameters were analyzed in 72 SLE patients and 63 healthy controls. Additionally, IL-36 cytokine mRNA levels were assessed in 30 of 72 SLE patients and 20 of 63 healthy controls using real-time quantitative reverse transcription polymerase chain reaction (RT-PCR). Compared to healthy controls, SLE patients had significantly decreased serum IL-36Ra levels (P = 0.001) and markedly increased serum IL-36α and IL-36γ levels (P = 0.004 and P = 0.001, respectively). Serum IL-36α and IL-36γ levels were significantly higher in active SLE patients [SLE Disease Activity Index (SLEDAI) score ≥ 5] than in inactive patients (SLEDAI score ≤ 4) (P = 0.020 and P = 0.017, respectively). Serum IL-36α and IL-36γ levels were strongly correlated with SLEDAI score (r = 0.308, P = 0.008 and r = 0.400, P = 0.001, respectively) and complement C3 levels (r = -0.276, P = 0.019 and r = -0.314, P = 0.007, respectively). Moreover, SLE patients with arthritis had significantly higher serum IL-36α and IL-36γ levels than those without arthritis (P = 0.001 and P 0.001, respectively). Our study indicates that the imbalanced antagonist/agonist profile of IL-36 cytokines may be linked to SLE pathogenesis. Furthermore, IL-36α and IL-36γ may participate in arthritis and may be good biomarkers of SLE disease activity.
- Published
- 2018
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