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Psoriatic plaques are characterized by epidermal hyperplasia and the presence of acute and chronic inflammatory cells. Active psoriatic plaques demonstrate a similar immunologic phenotype, as do ongoing cellular immune responses. Activated lymphocytes and other immune accessory cells have been detected within psoriatic plaques. Interleukin-2 receptor-positive and HLA-DR+ T cells are found in significantly higher numbers in active psoriatic plaques than in uninvolved skin or in treated plaques.1,2 The interleukin-2 receptor is a membrane protein that is present only on activated T cells and is associated with cell proliferation.3-5 HLA-DR is present on activated T cells but is also present on keratinocytes, macrophages, Langerhans cells, fibroblasts, dendritic cells, and endothelial cells in these lesions.1,2 The epidermal compartment is dramatically altered. The keratinocytes that are found in active plaques are HLA-DR+,1 γ-IP-10+,6 and I-CAM-1+,7 which is similar to the representation of these interferon gamma-induced proteins in

• Cyclosporine, an immunosuppressive drug, is effective in the treatment of recalcitrant psoriasis. Previous work suggested that keratinocyte hyperproliferation and inflammation are linked in psoriasis and that immune mechanisms participate in the pathogenesis of psoriasis. Transforming growth factor (TGF) α may be an important regulatory factor of epidermal growth as overproduction of TGF-α is associated with epidermal hyperplasia in psoriatic plaques and epidermal growth factor receptors are overexpressed in psoriatic epithelium. In this study, the effects of cyclosporine on cultured human keratinocytes were examined. Cyclosporine specifically inhibited keratinocyte cell-cycle progression in the G1 phase without causing keratinocytes to terminally differentiate. Cyclosporine did not decrease the expression of TGF-α or epidermal growth factor receptors. These results suggest that the effects of cyclosporine on psoriatic skin are unrelated to direct effects on autocrine growth regulation of keratinocytes via TGF-α production or of epidermal growth factor receptor modulation.(Arch Dermatol. 1991;127:1172-1179)

REPORT OF A CASE The patient, a 35-year-old bisexual man, was positive for the human immunodeficiency virus and was hospitalized with fever, weight loss, and severe abdominal pain. The patient had multiple hypopigmented and flesh-colored 1- to 3-mm papules, many with central umbilication, scattered on his face and neck.Cytologic examination of the material prepared from these lesions, by a variety of techniques described in detail below, suggested a presumptive diagnosis of cutaneous cryptococcosis.Subsequent histologic examination of a skin biopsy specimen showed a dermal mass of fungal organisms with abundant pale capsular material and little evidence of inflammatory reaction; the capsular material stained with mucicarmine (Figure, top). Fungal cultures of the skin biopsy specimen yielded Cryptococcus neoformans. Cryptococcal organisms were also identified in the blood, spinal fluid, and bone marrow specimens and in bronchial washings. Cerebrospinal fluid cryptococcal latex agglutination occurred at a dilution of 1:1024. Fluconazole was administered