CD8 T Cells and IFN-γ Emerge as Critical Players for Psoriasis in a Novel Model of Mouse Psoriasiform Skin Inflammation  Paola Di Meglio, João H. Duarte  Journal of Investigative Dermatology  Volume 133, Issue 4, Pages 871-874 (April 2013) DOI: 10.1038/jid.2012.426 Copyright © 2013 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 1 CD8 T cells mediate Ras-induced psoriasis-like skin inflammation through IFN-γ. Overexpression of activated Ras in suprabasal keratinocytes (KC) resulted in psoriasiform skin inflammation with skin acanthosis, hyperkeratosis, and intraepidermal neutrophil (N) and T-cell infiltration, including IL-17A+IFN-γ+ CD8+ T cytotoxic (Tc1/17) cells. Ras-overexpressing KCs might recruit Tc1/17 cells through the release of CXCL16 interacting with CXCR6 specifically expressed on CD8+ T cells, also possibly bearing very-late antigen (VLA-1) expression, which favors epidermal localization. Proinflammatory cytokines released by Tc1/17 cells, especially IFN-γ, enhance KC activation and proliferation, promoting KC production of neutrophil-attractant CXCL1 and S100 family members (S100A7, S100A8, and S100A9). Moreover, IFN-γ favors Th-17 and IL-17+ γδ-T-cell infiltration into the skin, possibly by programming dendritic cells to produce IL-17-driving cytokines IL-23 and IL-1 and chemoattracting CCL2 and MIP-2. Journal of Investigative Dermatology 2013 133, 871-874DOI: (10.1038/jid.2012.426) Copyright © 2013 The Society for Investigative Dermatology, Inc Terms and Conditions

Journal of Investigative Dermatology 2013 133, 871-874DOI: (10 Journal of Investigative Dermatology 2013 133, 871-874DOI: (10.1038/jid.2012.426) Copyright © 2013 The Society for Investigative Dermatology, Inc Terms and Conditions