Serum IL-21 levels are elevated in atopic dermatitis patients with acute skin lesions
Interleukin (IL)-21 is a member of the type I cytokine family and plays a role in the pathogenesis of T helper type 2 allergic diseases. It has been reported that IL-21 expression is upregulated in acute skin lesions in atopic dermatitis (AD) patients; however, little is known about the serum IL-21...
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Veröffentlicht in: | Allergology international 2017-07, Vol.66 (3), p.440-444 |
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Sprache: | eng |
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Zusammenfassung: | Interleukin (IL)-21 is a member of the type I cytokine family and plays a role in the pathogenesis of T helper type 2 allergic diseases. It has been reported that IL-21 expression is upregulated in acute skin lesions in atopic dermatitis (AD) patients; however, little is known about the serum IL-21 levels of AD patients. The aim of this study was to quantify the serum IL-21 levels of AD patients and to evaluate the relationships between the serum IL-21 level and disease severity, laboratory markers, and eruption type in AD patients.
We measured the serum IL-21 levels of adult AD patients and healthy control subjects using an enzyme-linked immunosorbent assay.
The adult AD patients exhibited significantly higher serum IL-21 levels than the healthy control subjects. A comparison of the patients' serum IL-21 levels based on the clinical severity of their AD revealed that the patients with severe AD demonstrated significantly higher serum IL-21 levels than those with mild AD and the healthy control subjects. The serum IL-21 levels were significantly correlated with the skin severity score, and especially with the degree of acute lesions such as erythema and edema/papules. The serum IL-21 level was not associated with laboratory markers, such as the serum IgE level, the serum thymus and activation-related chemokine level, blood eosinophilia, and the serum lactate dehydrogenase level.
These results suggest that IL-21 might be involved in the pathogenesis of AD, especially the development of acute skin lesions. |
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ISSN: | 1323-8930 1440-1592 |
DOI: | 10.1016/j.alit.2016.10.010 |