Supplementary Materials

The PDF file includes:

• Materials and Methods
• Fig. S1. Additional features of LC-mediated protection from UVR-induced keratinocyte apoptosis and skin injury.
• Fig. S2. The role of accumulated monocytes and monocyte-derived DCs in UVR-induced skin injury.
• Fig. S3. Additional features of LC-mediated protection of keratinocytes in vitro.
• Fig. S4. Mice treated with EGFR inhibitor resemble Langerin-DTA mice and timing of epidermal EGFR activation after UVR exposure.
• Fig. S5. Effect of human LCs on human keratinocytes without UVR and further characterization of in vitro LC-keratinocyte EGFR signaling.
• Fig. S6. Characterization of mouse and human ADAM17 expression, LC-Ad17 mice, and Langerin-Cre mice.
• Fig. S7. Effects of inducible ADAM17 deletion in LCs.
• Fig. S8. Validation of EGFR ligand release assay and characterization of keratinocyte EGFR ligand release.
• Fig. S9. Photosensitive MRL-Fas^lpr mice have more skin plasma cells and reduced LC EGFR ligand expression, LC ADAM17 activity, and LC EGFR ligand release.
• Fig. S10. B6.Sle1yaa mice exhibit photosensitivity and characterization of EGFR ligand expression by their LCs.
• Fig. S11. EGFR ligand application reduces the severity of UVR-induced skin lesions and lymph node B cell responses in SLE model mice.
• Fig. S12. Model of protective LC-keratinocyte axis and dysfunction of this axis in lupus photosensitivity.
• Fig. S13. Uncropped Western blot images.
• Table S1. List of primary antibodies.
• Table S2. Secondary antibodies and other staining reagents.
• Reference (53)

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Other Supplementary Material for this manuscript includes the following:

• Table S3 (Microsoft Excel format). Primary data.