J. B. O'Driscoll

Oestrogen receptor beta is the predominant oestrogen receptor in human scalp skin.

Abstract: Oestrogens play a major role in non‐classic target tissues in both sexes, yet there have been few studies on estrogens and skin. Recently a second oestrogen receptor (ERβ) has been discovered. Therefore, we have compared the expression of oestrogen receptor alpha (ERα), beta (ERβ), the androgen receptor (AR) and a cell proliferation marker in male and female non‐balding scalp skin. ERβ was the major steroid receptor expressed in human skin. It was highly expressed in epidermis, blood vessels and dermal fibroblasts, in contrast to ERα and AR. In the hair follicle, ERβ expression was localized to nuclei of outer root sheath, epithelial matrix and dermal papilla cells, in contrast to ERα, and the AR, which was only expressed in dermal papilla cells. Serial sections also showed strong nuclear expression of ERβ in the cells of the bulge, while neither ERα nor AR was expressed. In the sebaceous gland, ERβ was expressed in both basal and partially differentiated sebocytes. ERα exhibited a similar pattern of expression, while the AR was expressed in the basal and very early differentiated sebocytes. There was no obvious difference in the expression of either oestrogen receptor in male or female skin. The wide distribution of ERβ in human skin suggests that oestrogens may play an important role in the maintenance of skin and in the regulation of the pilosebaceous unit, and provides further evidence for oestrogen action in non‐classic target tissues. The differential expression of ERα, ERβ and AR in human skin suggests that the mechanisms by which steroid hormones mediate their effects may be more complex than previously thought.

A quantitative immunohistochemical study of the expression of integrins by nerves in psoriatic and normal skin

Summary Qualitative and quantitative assessment of integrin expression by dermal nerves was made by an avidin‐biotin immunoperoxidase method on snap‐frozen biopsies from affected psoriatic skin, and skin from normal control subjects with no history of skin disease. Nerves expressed α1, α2, α3, α6 β1 and β4 integrin subunits, and perineural sheaths in the mid‐dermis also expressed these subunits, with the exception of α2. There were more upper dermal nerve segments expressing αl integrin compared with other integrins both in controls and in psoriatic skin. The greater number of nerves expressing αl integrin compared with other integrins may be due to anatomical or functional differences between groups of nerves. There were significantly more nerves expressing αl, α2, α3, α6 and β4 integrins in psoriatic skin compared with control skin. This generalized increase may indicate a secondary trophic effect on all nerves rather than a specific increase in one type of nerve. However, the expression of α2 integrin may be significant in the pathogenesis of the psoriatic plaque, in that it was barely detectable in the normal site‐matched biopsies, but much greater in psoriatic plaques. The study of the expression of adhesion molecules by neurones in psoriasis offers a new avenue for investigation of the role of neuronal hypertrophy in the initiation and maintenance of psoriatic plaques.

Changes in numbers of epidermal cell adhesion molecules caused by oral cyclosporin in psoriasis.

AIM--To determine the effects of a three month course of low dose cyclosporin on the expression of epidermal cell adhesion molecules. METHODS--Eighteen patients with psoriasis were treated for 12 weeks with either 2.5 or 5 mg/kg/day of oral cyclosporin. Biopsy specimens taken from skin before, during, and after cyclosporin treatment were stained immunohistochemically for CD 54 (ICAM-1), CD 29 (beta-1 integrins), and CD18 (beta-2 integrins). RESULTS--There was a highly significant (p < 0.01) clinical response after 12 weeks of cyclosporin as assessed by the Psoriasis Area and Severity Index (PASI) score. The staining of CD 29 on keratinocytes of affected and unaffected psoriatic skin was not affected by cyclosporin. Epidermal CD54 was variably expressed in active psoriatic plaques and changed unpredictably after cyclosporin (p = NS). Staining for CD18 on large epidermal dendritic cells was reduced after cyclosporin (p < 0.02). The expression of CD18 by large epidermal dendritic cells during treatment correlated strongly with the PASI score at that time and one month after stopping cyclosporin (p < 0.02). CONCLUSIONS--Persistence of epidermal staining for CD 54 in psoriasis is compatible with a good clinical response to cyclosporin. Residual staining for CD 18 on large epidermal dendritic cells may be a useful marker for early clinical relapse.