UVB-Induced Skin Inflammation and Cutaneous Tissue Injury Is Dependent on the MHC Class I–Like Protein, CD1d Stephan Ryser, Marlène Schuppli, Beatrice.

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UVB-Induced Skin Inflammation and Cutaneous Tissue Injury Is Dependent on the MHC Class I–Like Protein, CD1d Stephan Ryser, Marlène Schuppli, Beatrice Gauthier, Dianelys R. Hernandez, Olivier Roye, Daniel Hohl, Bruce German, James A. Holzwarth, Angus M. Moodycliffe Journal of Investigative Dermatology Volume 134, Issue 1, Pages 192-202 (January 2014) DOI: 10.1038/jid.2013.300 Copyright © 2014 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 1 UVB-induced cutaneous tissue injury and inflammation are abolished in CD1d-knockout mice. (a) Photographs of single UVB-irradiated backs of CD1d knockout (CD1d−/−) and wild-type (WT) (C57BL/6 × 129) mice exposed to different UVB doses. (b) Hematoxylin and eosin staining of the backs of single UVB-irradiated C57BL/6 CD1d−/− and WT mice at 48 hours. Single arrowheads: inflammatory infiltrates; double arrowheads, black: epidermis erosion, white: intact epidermis. (c) Immunohistofluorescence of skin sections from (b) stained for myeloperoxidase (MPO) and 4,6-diamidino-2-phenylindole (DAPI). Dashed: epidermis–dermis junction. Small arrows: MPO-positive cells. Large arrow: epidermis ulceration. (d) Mean epidermal MPO staining (normalized to the total epidermal surface)±SE for WT (n=3) and CD1d−/− (n=4) skin sections; analysis of variance, **P<0.01. (e, d) Mean MPO-positive cells in the dermis (per 104 μm2)±SE. Scale bar=0.05 mm. Journal of Investigative Dermatology 2014 134, 192-202DOI: (10.1038/jid.2013.300) Copyright © 2014 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 2 UVB-induced pro-inflammatory gene expression is severely diminished in CD1d-knockout skin. (a, b) COX-2, tumor necrosis factor α (TNFα), IL-6, CXCL1, CXCL2, and CCL3 mRNA expression in the skin of UVB-irradiated C57BL/6 × 129 CD1d−/− (○) and wild-type (WT; •) mice. (a) mRNA levels measured at different time points after high-dose UVB (430 mJ cm−2) exposure. Non-irradiated (0 hours). (b) mRNA levels 72 hours after exposure to 86, 215, or 430 mJ cm−2 UVB. (c) Skin IL-6 and Ccl3 protein levels of C57BL/6 CD1d−/− (KO) versus WT mice at different times after exposure to 200 mJ cm−2 UVB. Non-irradiated (0 hours). *P<0.05 and **P⩽0.02. NS, no significance. Data are the means±SEM of triplicate wells; three independent experiments with n=5 per group. Journal of Investigative Dermatology 2014 134, 192-202DOI: (10.1038/jid.2013.300) Copyright © 2014 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 3 UVB-induced epidermal proliferation but not apoptosis is enhanced in CD1d-knockout skin. (a–d) TUNEL and immunofluorescence of UVB-irradiated skin sections from C57BL/6 wild-type (WT; n=3) and CD1d knockout (CD1d−/−) (n=4) mice after exposure to a single UVB dose (200 mJ cm−2). (a) Apoptotic cells (green), total cells (red). (b) Quantification of (a) mean % of apoptotic cells 24–72 hours after UVR, non-irradiated (0 hours); analysis of variance, ***P<0.001 compared with non-UV conditions; nonsignificant (NS) compared with the cell type. (c) Skin sections stained for Ki67 (red), epidermal cytokeratin (green), and 4,6-diamidino-2-phenylindole (DAPI). (d) Quantification of (c) mean % of Ki67+ keratinocytes in the stratum basal 24–168 hours after UVR, non-irradiated (0 hours). (e) Epidermal thickness (μm) of (c) 24–168 hours after UVR. Analysis of variance, ***P<0.001; **P<0.01; *P<0.05. Scale bar=0.05 mm. PI, propidium iodide. Journal of Investigative Dermatology 2014 134, 192-202DOI: (10.1038/jid.2013.300) Copyright © 2014 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 4 NKT cell-deficient mice are not resistant to UVB-induced cutaneous tissue injury and inflammation. (a) Hematoxylin and eosin (H&E) staining of single UVB-irradiated type I NKT cell-knockout mice (Jα18−/−) and wild-type (WT) mice backs 48 hours after exposure to 200 mJ cm−2 UVB. (b) Skin IL-6 and Ccl3 protein levels of (a) after exposure to 100 or 200 mJ cm−2 UVB. (c) H&E staining of UVB-irradiated type I and II NKT cell-deficient mice (TCRα−/−) and WT mice backs 48 hours after exposure to 200 mJ cm−2 UVB. (d) Skin IL-6, CCL3, and tumor necrosis factor α (TNFα) protein levels of (c). *P<0.05; NS, no significance. Data are the means±SEM of triplicate wells, two independent experiments with n=7–10 per group. Single arrowhead: inflammatory infiltrates. Double arrowhead: epidermis erosion. Non-irradiated (0 hours). Scale bar=0.05 mm. Journal of Investigative Dermatology 2014 134, 192-202DOI: (10.1038/jid.2013.300) Copyright © 2014 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 5 CXCL1 expression is reduced in CD1d−/− mouse epithelial keratinocyte (MEK) and differentiated myeloid cells. (a) ELISA of UVB dose-dependent release of CXCL1 by wild-type (WT) and CD1d knockout (CD1d−/−) MEK 24 hours after exposure (triplicates, means±SD), representative experiment performed three times independently. (b) ELISA of CXCL1 protein and (c) mRNA levels in resting WT and CD1d −/− MEKs. t-Test n=9, means; *P<0.05. Kinetic of CXCL1 (d) and mIL-6 (e) proteins released in the medium of WT and CD1d −/− bone marrow–derived dendritic cell (BMDC) stimulated with 100 ng ml−1 lipopolysaccharide (LPS) over 24 hours (ELISA triplicates; means±SD), representative experiment performed three times independently. (f) CXCL1 mRNA levels expressed in resting WT and CD1d −/−-deficient BMDCs and bone marrow–derived macrophages (BMDM); t-test n=6 for BMDC, n=8 for BMDM; means±SEM; *P<0.05. Journal of Investigative Dermatology 2014 134, 192-202DOI: (10.1038/jid.2013.300) Copyright © 2014 The Society for Investigative Dermatology, Inc Terms and Conditions