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Twenty-seven patients suffering from long-standing, severe, recurrent herpes simplex (14 labial and 13 genital) who had not responded adequately to prior therapy were recruited for this open, monitored study. They were treated with thymopentin 50 mg subcutaneously three times weekly for a period of 6 weeks. Clinical controls were performed once a week and then again 6 weeks after cessation of therapy; laboratory investigations were done at time points 0, 3, and 6 weeks. Additionally, information was collected with regard to the clinical course during the following year. Thirteen of 14 patients with labial infection and 10 of the 13 with genital herpes improved markedly (p less than 0.05) as shown by decrease in the relapse rate of at least 50%, shorter relapse episodes, and improvement of symptoms such as pain and itching. Fourteen of these 27 patients experienced no relapse for a period longer than 4 months after cessation of therapy. These favorable results were paralleled by a statistically significant increase in the T cell helper/suppressor ratio. This finding indicates that thymopentin acts as an immunodomulator; it is assumed that the activation of T helper cells induces-presumable via interleukin 2-the proliferation of cytotoxic T lymphocytes and natural killer cells which play a major role in the natural immune defense. No serious side effects of thymopentin were recorded.

Contact allergy to corticosteroids is more prevalent than previously recognized and often goes undetected. Nineteen patients with corticosteroid contact allergy are presented. Sixteen reacted to tixocortol pivalate and also to other corticosteroids, particularly to hydrocortisone, which could explain exacerbations of eczema in these cases. Tixocortol pivalate may be a useful marker for screening patients for contact sensitivity to several corticosteroids.

We wanted to evaluate the eventual expression of viral antigens and MHC class II products by keratinocytes as well as the alterations of epidermal Langerhans cells and dermal dendritic cells in viral lesions of skin and mucous membranes. Therefore we investigated 68 biopsy specimens of protracted viral lesions, such as warts, condylomas, and mollusca contagiosa, and of rapidly resolving viral lesions such as herpes simplex virus infection. For this we used immunohistochemical staining techniques and several monoclonal and polyclonal antisera. In most cases investigated viral antigens (human papilloma virus antigens or herpes simplex virus type 1 antigens) could be demonstrated in keratinocytic nuclei. Except for a few viral lesions in which epidermal Langerhans cells were rather numerous, epidermal Langerhans cells were reduced in number or absent in almost all viral lesions. Moreover, epidermal Langerhans cells and dermal dendritic cells showed changes in morphology, distribution, and immunophenotype. These alterations may be caused by a toxic effect of the virus on dendritic cells. HLA-DR+ keratinocytes could be identified in few viral lesions only; HLA-DQ+ keratinocytes were not seen. Possible explanations for this lack of MHC class II expression by keratinocytes are discussed.

Skin biopsies from 34 patients, presenting with a variety of bullous skin disorders were investigated, using routine light microscopy and immunohistochemistry. In bullous skin diseases characterized by deposition of complement factors (CF) and/or immunoglobulins (Ig), a monolayer of OKIa+1, OKT-6, OKM-1 dendritic cells was found at the dermo-epidermal junction. Retrospectively, these cells were easily recognized on paraffin embedded, H & E stained material. In bullous skin disorders, showing no deposition of CF and/or Ig, this monolayer of dendritic cells was lacking. It is suggested that these OKIa+1, OKT-6, OKM-1 dendritic cells at the dermo-epidermal junction represent some type of antigen presenting cells, not corresponding to Langerhans cells, veiled cells or indeterminate cells.

In this article are reviewed the various hypotheses concerning the etiology of the persistent light reaction and photosensitivity dermatitis, which occurs among older people and is characterized by an extreme photosensitivity that sometimes evolves into a pseudolymphoma, that is, actinic reticuloid. An etiologic agent can sometimes be demonstrated, but the precise pathogenetic mechanism is unknown. Clinical experience and experimental research indicate that the cause is most probably multifactoral: contact allergenic, photoallergenic, phototoxic, immunologic, and metabolic factors are involved, but their precise roles in the origin of the extreme photosensitivity are still unclear. Localized persistent light reactivity could result from the continued effects of the original photoallergen, but generalized photosensitivity is more difficult to account for. Among the many different hypotheses, two are of special interest: autosensitization of skin proteins with endogenous photosensitizers and cellular hypersensitivity to light, as is manifested by fibroblast cultures of actinic reticuloid patients.