ACKR2: Nature’s Decoy Receptor Lures Unsuspecting Chemokines in Psoriasis  Tomotaka Mabuchi, Samuel T. Hwang  Journal of Investigative Dermatology  Volume 137, Issue 1, Pages 7-11 (January 2017) DOI: 10.1016/j.jid.2016.09.035 Copyright © 2016 The Authors Terms and Conditions

Figure 1 Interferon-γ up-regulates ACKR2 at distant sites of inflammation. Schematic of experimental induction of psoriasiform dermatitis at an (a) primary site (site 1) only (left) or at a secondary site (site 2) after initial application of IMQ at site 1 (right), reprinted from Shams et al. (2017) with permission of Elsevier. (b) Systemic treatment with IFN-γ at the time of primary treatment with IMQ at site 1 results in a differential response to topical IMQ at site 2 compared with no systemic treatment. Namely, topical IMQ at site 1 plus IFN- γ treatment results in up-regulation of ACKR2 in the epidermis, decreases in T-cell infiltration in the epidermis, and reduction of epidermal hyperplasia and dermal inflammation. IMQ, imiquimod; WT, wild type. Journal of Investigative Dermatology 2017 137, 7-11DOI: (10.1016/j.jid.2016.09.035) Copyright © 2016 The Authors Terms and Conditions