Evaluation of Interleukin-9 Serum Level and Gene Polymorphism in A Sample of Systemic Lupus Erythematosus in Iraqi Female's Patients

Background: Immunological gene and serum level for interleukin- 9 rs 17317275 have been established to have linked to predisposition systemic lupus erythematosus (SLE) and its severity. SLE is a severe, systemic autoimmune disease characterized by autoantibody generation, complement activation, and immune complex deposition. In the pathophysiology of SLE, cytokines have a pleiotropic function. Recently, IL-9 was discovered to mediate strong anti-inflammatory effects in numerous cells or experimental autoimmune models.
Objective: This study aimed to determine the role of age, IL-9 serum level and genetic polymorphism, C-reactive protein (CRP), Anti-nuclear antibody (ANA) and Anti- double-stranded DNA (anti-dsDNA) to recognize SLE pathogenesis.
Materials and Methods: This case-control study was carried out in Baghdad Teaching Hospital and Typical Rheumatology Unit through the period from October 2021 to January 2022.103 Iraqi patients with SLE illness and 50 healthy Iraqis were included. Blood samples were taken. Serum IL-9 levels measured using the sandwich enzyme-linked immune-sorbent assay technology (ELISA) and cytokine genotyping by using allele-specific PCR technique
Results: SLE groups had greater levels of IL-9 than did healthy volunteer. Furthermore, both autoantibodies (ANA, Ant-dsDNA) were positive in SLE patients. The findings indicated that CRP was much higher in SLE subjects than those of healthy controls. On the other hand, the results showed that there was non-significance (p-value > 0.05) in age of studied groups. Concerning genotyping frequencies, the GG and AG genotyping were greater in the SLE group compared to the healthy subjects, while the AA genotyping frequency was significantly lower in the SLE group compared to the healthy people.
Conclusion: This study indicated the major roles of the serum level and genetic polymorphism of IL-9, CRP, ANA and anti-ds DNA in pathogenesis and severity of SLE.