Abstract
BackgroundIn this study, we aim to evaluate the balance of interleukin (IL)-33 and its soluble receptor sST2 in patients with aplastic anemia (AA).MethodsPlasma IL-33, IL-17 and sST2 levels were measured in patients with active AA (n = 31), AA in remission (n = 29) and in healthy subjects (n = 30), using enzyme linked immunosorbent assays (ELISAs).ResultsThe results showed that sST2 and IL-17 levels were significantly elevated in patients with active AA when compared to control subjects, but IL-33 levels were significantly lower in AA patients, which resulted in elevated sST2/IL-33 ratios in patients with active disease. During remission stages, the levels of these cytokines were comparable to those of healthy controls.ConclusionsThe elevated levels of sST2/IL-33 in the plasma during active stages of the disease suggest a possible role in the pathogenesis and course of AA.
Highlights
In this study, we aim to evaluate the balance of interleukin (IL)-33 and its soluble receptor sST2 in patients with aplastic anemia (AA)
It has become evident that T helper 1 (Th1) and Th2 cells have pathogenic importance in AA; activated antigen-presenting cells (APCs), dendritic cells (DCs), may promote polarization to Th1 cells and activate cytotoxic T lymphocytes (CTLs)
Plasma sST2 levels of AA patients with active disease were significantly higher compared with healthy controls (1370.1 ± 530.3 vs. 903.7 ± 329.3 pg/ml, P < 0.01; Fig. 1b)
Summary
We aim to evaluate the balance of interleukin (IL)-33 and its soluble receptor sST2 in patients with aplastic anemia (AA). Acquired aplastic anemia (AA) is primarily considered an immune-mediated bone marrow failure syndrome, which differs from the other conditions associated with inherited mechanisms [1]. A variety of immune molecules, including interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α) and interleukins (ILs) produced by DCs, T lymphocytes. Like IL-1, IL-33 appears to act as a dual function cytokine with both nuclear and extracellular effects [8]. Like other members of the IL-1 receptor family, ST2 exists in a soluble form (sST2), generated by alternative mRNA splicing, which acts as a decoy receptor to inhibit IL-33 signaling [7]. Over the last several years, several studies have suggested that IL-33 and sST2 are involved in immune diseases such as systemic lupus erythematosus and atopic dermatitis [8,9,10]
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