Decreased expression of IL-33 in immune thrombocytopenia

• IL-33 was down-regulated in plasma of ITP patients while its soluble receptor was up-regulated.
• The discrepancy expression of IL-33 and sST2 was obvious in ITP patients with active disease.
• sST2 mRNA was up-regulated in active ITP patients.
• sST2/IL-33 ratio in active ITP patients was increased compared with the normal and remission groups.

PurposeInterleukin-33 (IL-33) is an IL-1 family cytokine which signals via its ST2 receptor and is involved in several autoimmune diseases by regulating T cell immune responses. This study aims to measure the expression of soluble ST2 (sST2) and IL-33 in active immune thrombocytopenia (ITP) and during remission.MethodsThirty-two ITP patients with active disease and 20 patients in remission were studied. IL-33 and sST2 were measured in plasma using ELISA and compared with 27 age- and sex-matched healthy controls. Real-time quantitative PCR was used to determine IL-33 and sST2 mRNA expressions.ResultsThe IL-33 level in plasma was significantly down-regulated in the patients with active ITP (P < 0.01). The sST2 level was up-regulated (P < 0.01) in the patients with active ITP compared with ITP in remission and the normal controls. No significant changes were detected between the patients with ITP in remission and the normal controls. We detected an obvious up-regulation of sST2 mRNA levels but no change in IL-33 mRNA expression. There was no correlation observed between IL-33 or sST2 expression and the platelet count of the patients with active ITP. The plasma and mRNA level ratios of sST2/IL-33 were up-regulated in the active disease patients (P < 0.01). However, no difference was detected between the ITP patients with remission disease and healthy controls.ConclusionsThe values of sST2 and IL-33 observed in patients with ITP correlated with disease activity. Considering the role of IL-33 in regulating T cell immunity, studies on IL-33 and sST2 in ITP would further improve our understanding of the pathogenesis of ITP.