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The IFN-I signature characterizes an early and transient event in its progression and a link between the innate and adaptive immune response.65 Studies have shown that IFNα, produced mainly by plasmacytoid dendritic cells (pDCs), stimulates the production of chemokines, such as CXCL9 and CXCL10, by keratinocytes, leading to the recruitment of T-cells expressing their receptor: CXCR3.65,72 Furthermore, HSP70 potentially contributes to skin inflammation by activating pDCs and increasing IFNα secretion.72 Cytotoxic CD8+ T-cells are necessary and sufficient for the destruction of melanocytes, acting as an effector arm of autoimmunity.78 The lesions are caused by effector CD8+ T-lymphocytes in the initial or active phase of the disease and by recirculating and resident memory CD8 + T (TEM) lymphocytes in the stable phase

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