Dopa reaction of fetal melanocytes before and after skin transplantation on to nude mice

Abstract

We have previously demonstrated that human fetal epidermal melanocytes are dopa-negative. The present study was conducted to test the hypothesis that human fetal melanocytes can be activated to produce melanin under conditions differing from their natural in utero environment. To address this question, dopa staining activity of fetal epidermal sheets, obtained from seven aborted fetuses with estimated gestational ages of 13-20 weeks, was evaluated before and after engraftment on to nude mice. Dopa staining became positive 7 days post-engraftment. The intensity of the dopa reaction and the mean number of melanocytes increased by day 14 post-engraftment, and these changes were even greater by day 30. These observations indicate that human fetal melanocytes, potentially capable of synthesizing melanin under conditions differing from their normal in utero environment, are either inhibited, or not stimulated to do so.

What causes alopecia areata?

“…This study confirmed an association of AA with NKG2D‐activating MICA family members, most notably ULBP3, and overexpression of NKG2D ligands in patients with AA . Shortly thereafter, the first functional proof for the importance of IFNg‐secreting NKG2D + cells in AA pathogenesis was provided by a new humanized mouse model of AA .…”

Coenzyme Q10 enhances dermal elastin expression, inhibits IL‐1α production and melanin synthesis in vitro

“…3B). Furthermore, DOPA staining, as a morphological indicator of tyrosinase activity [25], confirmed the decreased tyrosinase activity following CoQ 10 treatment (Fig. 3C).…”

Deletion of the activating NKG2C receptor and a functional polymorphism in its ligand HLA‐E in psoriasis susceptibility

“…Interestingly, we have previously found that there is an expansion of NKG2A+ NK cells within psoriatic skin (20). An important role for NK cell receptors in cutaneous autoimmune disease is also observed in studies of alopecia areata, in which the interaction of the activating NK receptor NKG2D with its ligands MICA and ULBP3 leads to immune attack of the hair follicle (21)(22)(23).…”