Increased Activity and Number of Epidermal Melanocytes in Lesional Psoriatic Skin

Abstract

Background: Psoriatic lesions may resolve with hypo- or hyperpigmentation. The involvement of melanocytes in this dichotomous clinical outcome is not fully investigated. Objectives: Qualitative and quantitative assessment of melanocytes in untreated lesional and non-lesional psoriatic skin (n = 15) and healthy controls (n = 10). Methods: Skin biopsies were labelled immunohistochemically (APAAP technique) with the antimelanocyte monoclonal antibodies (MoAbs) HMB45, Melan A, tyrosinase and microphthalmia-associated transcription factor (MITF). The labelled melanocytes were evaluated by an independent investigator with a digital image analyser. Results: Lesional melanocytes, in contrast to those in non-lesional and healthy skin, exhibited features of activation in the form of dilatation, prominent and long dendrites and intense labelling. The number of melanocytes was significantly increased in psoriatic lesions in comparison with non-lesional psoriatic and healthy skin as shown by counts of cells labelled with the MoAbs HMB45 (3-fold; p < 0.001), Melan A (1.6-fold; p < 0.01) and tyrosinase (1.5-fold; p < 0.01). In contrast, labelling with MITF revealed no significant difference (1.2-fold increase; p > 0.05). Likewise, no significant difference between non-lesional psoriatic and healthy skin control was found (p > 0.05). Furthermore, no positively labelled dermal cells were detected, apart from few only detected with Melan A. Conclusions: Epidermal melanocyte activity and numbers are increased in the epidermal compartment of psoriatic lesions providing an explanation for postinflammatory hyperpigmentation.

Type-1 cytokines regulate matrix metalloprotease-9 production and E-cadherin disruption to promote melanocyte loss in vitiligo

“…This contrasts with lesional psoriatic skin, which harbors a high proportion of proliferating melanocytes, explaining not only the absence of complete depigmentation in patients despite melanocyte detachment from the basal layer of the epidermis, but also the fact that depigmented lesions are able to recover rapidly under therapies. This is consistent with previous reports showing an increased number of melanocytes both in psoriasis lesions and in resolved psoriasis skin (40,41).…”

UCHL1/PGP 9.5 Dynamic in Neuro-Immune-Cutaneous Milieu: Focusing on Axonal Nerve Terminals and Epidermal Keratinocytes in Psoriatic Itch

“…Melanocytes in the epidermis are located in the basal layer, while their prominent and long dendrites penetrate to the upper epidermal compartments participating in melanin transfer to the surrounding keratinocytes [ 44 ]. In psoriasis, melanocytes are elevated; however, MITF expression was noted to be comparable to controls [ 45 ]. The attention should be also focused to other studies where model of experimental skin injury demonstrated participation of PGP 9.5 with other axonal transport factors in synaptic cargo vesicles from DRG bodies to the periphery [ 46 ].…”

Current knowledge on autoantigens and autoantibodies in psoriasis

“…However, the question remains whether IL‐17 and TNF produced by pathogenic CD8 + T cells are solely responsible for reducing melanogenesis or whether other resident IL‐17 and TNF producing cells have this effect. A recent immunohistochemistry analysis showed that lesional melanocytes, opposed to those in non‐lesional and healthy skin, displayed longer and prominent dendrites and were significantly increased in numbers 28 . Accordingly, this increased melanocytic activity possibly explains the ability of melanocytes to directly activate Vα3S1/Vβ13S1 CD8 + T cells through tissue‐specific autoantigen presentation 10,12,28 .…”

“…A recent immunohistochemistry analysis showed that lesional melanocytes, opposed to those in non‐lesional and healthy skin, displayed longer and prominent dendrites and were significantly increased in numbers 28 . Accordingly, this increased melanocytic activity possibly explains the ability of melanocytes to directly activate Vα3S1/Vβ13S1 CD8 + T cells through tissue‐specific autoantigen presentation 10,12,28 . In addition to melanocytes, ADAMTSL5 is expressed in keratinocytes and perivascular dermal cells 29 .…”