Cumulatively, our results suggest that IL-25 levels are increased in patients with SLE and associated with disease activity; IL-25 plays a potent immunosuppressive role in the pathogenesis of SLE by suppressing the production of inflammatory cytokines.
This study demonstrated that the IL-9, IL-10 and IL-25 had significantly increased expressions in SLE-LN, followed by SLE without LN, compared to healthy controls.
Our results revealed that IL-12B rs17860508 and IL-27 haplotype CG are genetic risk factors for SLE and that both IL-12B rs17860508 and rs3212227 predict disease phenotype.
Disease type-stratified subgroup analysis yielded increased risk of related diseases in IL-27rs181206 T>C carriers in the allele model in immune thrombocytopenia (ITP), asthma, and esophageal cancer (EC) subgroups (ITP: OR=0.69, 95%CI=0.53~0.88, P=0.004; asthma: OR=0.60, 95%CI=0.41~0.89, P=0.010; EC: OR=0.79, 95%CI=0.64~0.97, P=0.026); and IL-27rs153109 A>G polymorphism was remarkably associated with the increased risk of related diseases in the allele model in ovarian cancer (OC), systemic lupus erythematosus (SLE), tuberculosis (TB), ulcerative colitis (UC), and chronic obstructive pulmonary disease (COPD) subgroups (all P<0.05).