Vitiligo, a disease presenting as white patches on the skin, is caused by selective destruction of melanocytes, which are completely absent in established lesions. In cases of active vitiligo, keratinocytes show vacuolar degeneration, especially in perilesional skin.1 This substrate degeneration might account for absence of melanocytes in vivo. There is apparently a close relationship between melanocytes and keratinocytes that is important for melanocyte survival and differentiation and that may involve keratinocyte-mediated cytokines. Granulocyte-monocyte-colony stimulating factor (GM-CSF) (a keratinocyte-derived melanocyte growth factor found in UV-A–induced melanosis), basic fibroblastic growth factor (bFGF) (a natural mitogen for melanocytes also produced by keratinocytes), and the stem-cell factor (SCF) c-KIT pathway (mediated by keratinocytes) all play a critical role in the control of melanocyte homeostasis.2,3 Furthermore, keratinocytes synthesize interleukin (IL) 1α, IL-6, tumor necrosis factor α (TNF-α), and transforming growth factor β (TGF-β), which are paracrine inhibitors of human melanocyte proliferation and melanogenesis.2
Moretti S, Spallanzani A, Amato L, Hautmann G, Gallerani I, Fabbri P. Vitiligo and Epidermal Microenvironment: Possible Involvement of Keratinocyte-Derived Cytokines. Arch Dermatol. 2002;138(2):273–274. doi:10.1001/archderm.138.2.266
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