Abstract
BackgroundTh2 cells play an important role in intermittent allergic rhinitis (IAR). Interleukin (IL)-33 stimulates the production of Th2-associated cytokines. IL-33 binds to ST2 receptor which is highly expressed on mast cells and selectively on Th2 cells. IL-33 and ST2 might be involved in the Th2-mediated immune response.ObjectiveWe analyzed the serum level of IL-33 and its receptor ST2 in patients with IAR sensitive to grass and/or tree pollen to assess if the serum level of IL-33 and/or ST2 may be a marker of the disease severity.MethodsIL-33, ST2 and total immunoglobulin (Ig) E were measured in sera of patients with IAR sensitive to birch and/or grass pollen and in patients with controlled bronchial asthma and in non-allergic controls. IAR severity was assessed by total nasal symptom score.ResultsSerum levels of IL-33 in patients with IAR were comparable with patients with bronchial asthma and were significantly higher in patients with IAR (P = 0.0035) and in patients with bronchial asthma (P = 0.008) than in controls. Serum levels of IL-33 correlated with disease severity.ConclusionElevated level of IL-33 in sera of patients with IAR sensitive to tree and/or grass pollen and the correlation of IL-33 with the disease severity suggest that IL-33 is involved in the pathogenesis of intermittent allergic rhinitis.
Highlights
Allergic diseases are thought to be Th2 cell-mediated diseases
We analyzed the serum level of IL-33 and its receptor ST2 in patients with intermittent allergic rhinitis (IAR) sensitive to grass and/or tree pollen to assess if the serum level of IL-33 and/or ST2 may be a marker of the disease severity
Serum levels of IL-33 in patients with IAR were comparable with patients with bronchial asthma and were significantly higher in patients with IAR (P = 0.0035) and in patients with bronchial asthma (P = 0.008) than in controls
Summary
Allergic diseases are thought to be Th2 cell-mediated diseases. Th2 cells produce cytokines, such as interleukin (IL)-4, IL-5 and IL-13. It has been shown that a novel cytokine, IL-33, is involved in the Th2-mediated immune response and stimulates the production of Th2associated cytokines. IL-33 is produced by mast cells after immunoglobulin (Ig) E-mediated activation and is able to trigger mast cells to release proinflammatory cytokines in vitro [2,3,4,5]. ST2 is highly expressed on mast cells and selectively on Th2 cells [6,7,8]. The IL-33/ST2 signalling pathway activates airway eosinophils that exacerbate airway inflammation in an autocrine and paracrine manner [11]. IL-33 binds to ST2 receptor which is highly expressed on mast cells and selectively on Th2 cells. IL-33 and ST2 might be involved in the Th2-mediated immune response
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