Abstract

Thymic stromal lymphopoietin (TSLP) is overexpressed in esional keratinocytes in atopic dermatitis (AD). The local increase n TSLP is associatedwith activation of dendritic cells which trigger he differentiation of naive CD4+T cells into proallergic CD4+Th2 ells. Thus, TSLP is thought to play an important role in the pathoenesis of AD, but the alteration of TSLP expression after treatment as not fully been understood. Here we investigated whether TSLP xpression in normal human epidermal keratinocytes (NHEKs) ould be affected by common clinical treatments including ultraiolet (UV) A and B, glucocorticosteroid, and calcineurin inhibitors. e first confirmed that TNF–alpha induced TSLP expression in HEKs by real–time PCR and ELISA. In addition, immunohistohemistry showed that TNF–alpha–positive cells were infiltrated n AD lesions. Next we observed that treatments of UVA (0.5, 1, 2, nd 5 J/cm2) significantly suppressed the induction of TSLP expresionby stimulationwithTNF-alpha (10ng/ml) in adose–dependent anner. A synthetic glucocorticosteroid dexamethasone (10−7, 0−6, and 10−5 M) and a calcineurin inhibitor tacrolimus (10−7, 0−6, and 10−5 M) also suppressed TSLP expression in NHEKs in dose–dependent manner. On the other hand, UVB (0.02, 0.04, .06, 0.08, and 0.1 J/cm2) induced TSLP expression in NHEKs. These echanisms might be associated with the clinical improvements nd further studies are needed to clarify the effects of UVB on TSLP xpression.

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