These results suggest that PEG may induce TH2 cells in the skin through the production of CCL17 by Langerhans cells and would explain the role of colonization by S aureus in patients with atopic dermatitis.
These results suggest that the -431C>T SNP of the TARC gene enhances the promoter activity of TARC gene but is not associated with susceptibility to AD in Japanese population.
Both TARC and CTACK serum levels in patients with AD were significantly higher than those in healthy control subjects and patients with allergic respiratory disease.
Our results suggest that the primary Th2-dominated inflammatory reaction in AD induced by TARC leads to an augmented skin-specific inflammatory reaction through CTACK.
Our results suggest that the primary Th2-dominated inflammatory reaction in AD induced by TARC leads to an augmented skin-specific inflammatory reaction through CTACK.
The purpose of this study was to investigate serum levels of Th2 chemokines TARC and MDC and a Th1 chemokine Mig in the same samples from patients with AD and their clinical correlation.
Furthermore, we found that TARC and MDC levels are significantly increased in the sera obtained from patients with atopic dermatitis, and that the amounts are correlated with the severity of atopic dermatitis.
The purpose of this study was to examine the expression and distribution of TARC and CCR4 mRNAs in samples of AD (n=15, acute lesions 8, chronic lesions 7) and normal skin (n=6).
Th2-specific chemokine thymus and activation-regulated chemokine (TARC)/CC chemokine ligand (CCL)17 is highly implicated in the pathogenesis of Th-2-dominated allergic diseases such as bronchial asthma (BA) and atopic dermatitis (AD).
TGF-beta1 inhibited IFN-gamma and TNF-alpha-induced TARC production in HaCaT cells via Smad2/3, suggesting that modulation of TGF-beta/Smad signaling pathway may be beneficial for the treatment of atopic dermatitis.