Abstract
Atopic dermatitis (AD) is a chronic inflammatory skin disease that is characterized by recurrent dermatitis, itchiness and high serum levels of IgE. CCL17 and CCL22 are the chemokines that attract and activate CCR4+ cells. We found the monocyte- derived dendritic cells (MoDCs) of AD patients secreted high levels of both CCL17 and CCL22. The toll-like receptor (TLR) family consists of 13 members and several ligands recognized by the TLR family have been identified. TLR2, for example, responds to lipoproteins and peptidoglycans (PGNs) from gram-positive bacteria, whereas TLR4 mediates LPS induces the production of pro-inflammatory and immune-related cytokines. Staphylococcus aureus is also reported to contribute to the exacerbation of AD skin lesion. We performed in vitro experiments to investigate the spontaneous production of CCL17 and CCL22 production by MoLCs. We next examined the effects of toll like receptor agonists on the production of Th2 chemokines by the MoLCs of AD patients. The present study was approved by the ethical committee of Saitama Medical University. We first examined whether the MoLCs of AD patients and HCs produced the CCL17 and CCL22 chemokines. We confirmed that the average amounts of CCL17 and CCL22 were significantly higher in AD patients than in HCs (p<0.01, p<0.01, respectively). We next examined whether the TLR ligands induce CCL17 and CCL22 production by the MoLCs of AD patients. LPS, Pam3CSK4 and poly I:C tended to increase the production of CCL17 and CCL22, while PGN was found to significantly enhance the production of both CCL17 and CCL22 in the MoLCs of AD patients. These data suggest that atopic inflammation is strongly influenced by innate immunity and that these molecules will be the target in the future treatment of atopic dermatitis.
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