Systemic-onset juvenile idiopathic arthritis (JIA) is speculated to follow a biphasic course, with an initial systemic disease phase driven by innate immune mechanisms and interleukin-1β (IL-1β) as a key cytokine and a second chronic arthritic phase that may be dominated by adaptive immunity and cytokines such as IL-17A.
Genomic DNA of 55 Iranian patients with JIA and 140 controls were extracted and typed for IL-1α gene at position -889, IL-1β gene at positions -511 and +3962, IL-1R gene at position Pst-I 1970, and interleikin-1 receptor antagonist (IL-1Ra) gene at position Mspa-I 11100, using polymerase chain reaction with sequence-specific primers method, and compared between patients and controls.
Clinical laboratory data and serum IL-1β of JIA patients were evaluated by medical chart review and enzyme-linked immunosorbent assay (ELISA), respectively.
It also underlines the genetic contribution of IL-1 polymorphisms to the pathogenesis of JIA, as another polymorphism within the IL-1beta may influence the risk of the disease.
The pathogenesis, clinical course, and response to treatment in systemic juvenile idiopathic arthritis (SJIA) differ from other types of juvenile idiopathic arthritis and are similar to other interleukin-1 (IL-1)-mediated diseases.
Interleukin (IL)-1α and IL-1β are proinflammatory cytokines that play a role in many diseases such as rheumatoid arthritis, juvenile rheumatoid arthritis, gout, and periodic inflammatory syndromes, including familial Mediterranean fever and Muckle-Wells syndrome.