Pathophysiologic role of Interleukin-33/ST2 in Sjögren's syndrome

Interleukin-33 (IL-33) is a member of the IL-1 family and has dual functions as nuclear factor well cytokine. The pivotal role IL-33 an active player contributing to aberrant local systemic damage been highlighted in several inflammatory autoimmune diseases. Primary Sjogren's syndrome (pSS) disease characterized by dry eyes mouth due dysfunctions exocrine glands, but also accompanied with manifestations. pathophysiology pSS advocated conjecture activated B T cells production cytokines autoantibodies, driving epithelial tissue progression. In pSS, released extracellular space from damaged salivary upon pro-inflammatory stimuli and/or dysfunction barrier. Counter-regulatory mechanisms are initiated limit actions portrayed increase decoy receptor for IL-33, soluble form ST2 (sST2). associated diseases, levels significantly elevated serum or tears patients. Mechanistically, acts synergy IL-12 IL-23 on NK NKT boost IFN-γ inflammation. TNF-α, IL-1β turn further activation IL-33/ST2 pathway, thereby constituting vicious loop leading exacerbation. axis involved opens new perspectives therapeutic target one culprits perpetuation.