CCL27–CCR10 interactions regulate T cell–mediated skin inflammation

✍ Scribed by Homey, Bernhard; Alenius, Harri; Müller, Anja; Soto, Hortensia; Bowman, Edward P.; Yuan, Wei; McEvoy, Leslie; Lauerma, Antti I.; Assmann, Till; Bünemann, Erich

• Book ID: 109926857
• Publisher: Nature Publishing Group
• Year: 2002
• Tongue: English
• Weight: 718 KB
• Volume: 8
• Category: Article
• ISSN: 1078-8956
• DOI: 10.1038/nm0202-157

✦ Synopsis

The skin-associated chemokine CCL27 (also called CTACK, ALP and ESkine) and its receptor CCR10 (GPR-2) mediate chemotactic responses of skin-homing T cells in vitro. Here we report that most skin-infiltrating lymphocytes in patients suffering from psoriasis, atopic or allergic-contact dermatitis express CCR10. Epidermal basal keratinocytes produced CCL27 protein that bound to extracellular matrix, mediated adhesion and was displayed on the surface of dermal endothelial cells. Tumor necrosis factor-alpha and interleukin-1beta induced CCL27 production whereas the glucocorticosteroid clobetasol propionate suppressed it. Circulating skin-homing CLA+ T cells, dermal microvascular endothelial cells and fibroblasts expressed CCR10 on their cell surface. In vivo, intracutaneous CCL27 injection attracted lymphocytes and, conversely, neutralization of CCL27-CCR10 interactions impaired lymphocyte recruitment to the skin leading to the suppression of allergen-induced skin inflammation. Together, these findings indicate that CCL27-CCR10 interactions have a pivotal role in T cell-mediated skin inflammation.