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The IL-33/sST2 Axis in Thromboangiitis Obliterans
Hiva Sharebiani1, Mehran Mohareri1, Ali Mirhosseini1
1Immunology Research Center, Inflammation and Inflammatory Diseases Division, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Journal of Inflammation Research
|August 9, 2020
Summary
Interleukin-33 (IL-33) levels are significantly elevated in thromboangiitis obliterans (TAO) patients, particularly during active disease phases. This IL-33/sST2 ratio differs from autoimmune vasculitis, suggesting a unique inflammatory pathway in TAO.
Area of Science:
- Immunology
- Rheumatology
- Vascular Medicine
Background:
- Thromboangiitis obliterans (TAO) classification remains debated, with uncertainty regarding its relation to systemic vasculitis.
- Elevated levels of Interleukin-33 (IL-33) and its decoy receptor sST2 are characteristic of the acute phase in systemic vasculitis.
Purpose of the Study:
- To investigate the serum levels of IL-33 and sST2 in patients with TAO.
- To compare these levels with those in healthy smokers and non-smokers.
- To explore the potential role of IL-33/sST2 in TAO pathogenesis and its distinction from autoimmune vasculitis.
Main Methods:
- Serum IL-33 and sST2 levels were measured in 50 TAO patients and 2 control groups (20 smokers, 19 non-smokers).
- Patients were categorized into active and quiescent disease phases, and by presence of gangrene or non-healing ulcers.
- Statistical analysis was performed to compare IL-33 and sST2 levels and the IL-33/sST2 ratio between groups.
Main Results:
- TAO patients exhibited significantly higher serum IL-33 levels compared to both control groups (p < 0.001).
- IL-33 levels were notably higher in the active phase of TAO and in patients with gangrene.
- The IL-33/sST2 ratio was significantly elevated in TAO patients across all disease phases compared to controls (p < 0.001).
Conclusions:
- The IL-33/sST2 regulation pattern in TAO differs from that observed in autoimmune vasculitis.
- These findings suggest that IL-33 may play a distinct role in the inflammatory processes underlying TAO.
