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Furthermore, HSP70 could be considered a potential marker to evaluate disease activity.3,5,6 On the other hand, MxA protein (human mixovirus resistance protein 1), inducible by IFN-, shows strong expression in active perilesional vitiligo skin, suggesting a contributing effect of IFN- in disease progression.7 Similarly, S100B is another DAMP released by damaged melanocytes, whose levels are increased in active vitiligo and can stimulate inflammatory responses.8 Also, high-mobility group box 1 (HMGB1) proteins can induce the production of chemokine ligands, such as CXCL1 or IL-8 by keratinocytes, acting in the recruitment of immune cells.9 Calreticulin (CRT) is another of the most studied molecules in vitiligo, as it induces melanocyte apoptosis and the release of membrane degradation products important for immunogenicity.10 Melanocyte adhesion deficiency Several research groups have demonstrated that melanocytes in vitiligo exhibit reduced adhesive properties

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Javeri H, Xiao L, Rohren E, Lee JH, Liao Z, Hofstetter W, Maru D, Bhutani MS, Swisher SG , Macapinlac H, Wang X, Ajani JA

8d,e), and M2 macrophage decrease (Supplementary Fig