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.
We identified unique signatures for AD (Immunoglobulin E (IgE), thymus- and activation-regulated chemokine (TARC) and macrophage-derived chemokine (MDC)), CD (10 proteins), and PS (kynureninase (KYNU)).
We examined plasma LIGHT levels, total serum IgE, serum value of CCL17 and peripheral blood eosinophil counts in patients with AD and healthy subjects.
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.
We found that AD S. aureus<sup>+</sup> patients had more severe disease based on all scoring systems except itch (Numerical Rating Scale), and they had higher levels of type 2 biomarkers (eosinophil count, tIgE, CCL17, and periostin).
We aimed to investigate the effects of DHE-Glc, a synthetic molecule derived from ergosterol, on AD-like skin lesions induced by 2,4-dinitrochlorobenzene (DNCB) in mice and to elucidate the effects of DHE-Glc on TNF-α/IFN-γ-induced production of CCL17 and CCL22 in human keratinocytes (HaCaTs) and DNCB induced skin inflammation mice model.
T<sub>H</sub>2 chemokines (CCL13, CCL17) were consistently elevated in patients with AD across all ages (P < .05), whereas T<sub>H</sub>1 (CXCL10) and T<sub>H</sub>17 (KYNU, CCL20) markers incrementally increased with age in both patients with AD and healthy subjects.
Oral administration of L. chungangensis CAU 28(T) suppressed the production of IL-4, IL-5, IL-12, IFN-γ, tumor necrosis factor-α, and thymus- and activation-regulated chemokine (TARC) in skin lesions, indicating that it strongly drives the local immune system with efficacy comparable to that of tacrolimus, a topical immunomodulatory drug used for the treatment of atopic dermatitis.
Levels of inflammatory cytokines and chemokines, such as thymus- and activation-regulated chemokine (TARC), macrophage-derived chemokine, and thymic stromal lymphopoietin (TSLP), were examined in human keratinocytes supplemented with or without CTP under AD-like inflammation.
IL-4 Augments IL-31/IL-31 Receptor Alpha Interaction Leading to Enhanced Ccl 17 and Ccl 22 Production in Dendritic Cells: Implications for Atopic Dermatitis.
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).
These findings indicate that Glyteer may exhibit therapeutic potential for AD by downregulating the CCL17 and CCL22 production from DCs in a Th2-deviated microenvironment.
The Th9 cell percentage, PU.1 and IL-9 expression levels of AD patients were all increased significantly compared with the other two control groups (P < 0·01), and correlated positively with SCORing Atopic Dermatitis index, serum immunoglobulin (Ig)E and thymus- and activation-regulated chemokine (TARC) levels (P < 0·05).
Among the biomarkers tested, serum SCCA2 also showed the best correlations with clinical AD severity and TARC and showed the best diagnosability for AD in ROC analysis.
Th2-related chemokines such as thymus and activation-regulated chemokine (TARC/CCL17) and macrophage-derived chemokine (MDC/CCL22), and pro-inflammatory cytokines including interleukin (IL)-1β and IL-6 are considered to play a crucial role in AD.
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.
Chemokines are important mediators of cell migration, and thymus and activation-regulated chemokine (TARC/CCL17) and macrophage-derived chemokine (MDC/CCL22) are well-known typical inflammatory chemokines involved in atopic dermatitis (AD).
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.