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T lymphocytes infiltrate the epidermis and follicular epithelium adhering to keratinocytes within hours following induction of cutaneous inflammation. To determine if the physical binding interaction between a T cell and keratinocyte induces transmission of activation pathways, CD3+ T cells (HUT 78) were allowed to directly bind to non-cytokine-treated cultured keratinocytes. When these T cells bound to keratinocytes, the keratinocytes were activated as evidenced by detection of tumor necrosis factor-alpha, interleukin-6, and intercellular adhesion molecule-1 mRNA. This induction was relatively mRNA specific, as several other mRNA were not found to be altered. This activation process appeared to be one-sided, as no change in HUT cell mRNA levels was detectable. The keratinocyte activation process was confined to cultures that had direct physical binding by HUT cells, because co-culturing the HUT cells immediately above the keratinocyte monolayer (but not in direct contact), resulted in no such mRNA alterations. This direct adhesion-mediated activation of keratinocytes by T lymphocytes may be important in the genesis of cutaneous inflammation by amplifying the original stimulus, as well as contributing to the trafficking pattern of inflammatory cells as they leave the general circulation and enter the skin.

Psoriatic skin lesions contain HLA-DR positive T lymphocytes, and other activation antigens, which suggest that the T cells may be producing lymphokines. Gamma interferon is produced by activated T cells, and its presence in psoriasis has been inferred by the lesional keratinocyte expression of 3 gamma interferon-inducible proteins i.e. HLA-DR, intercellular adhesion molecule-1, and gamma-IP-10. To determine whether gamma interferon is being produced directly in psoriatic lesions, punch biopsies of normal and diseased skin were separated into epidermal sheets and dermal fragments. Total cellular RNA was isolated from each epidermal and dermal compartment, and reverse transcribed followed by amplification of the resultant DNA by polymerase chain reaction. The amplification process involved the use of 5' and 3' primers for gamma interferon, and tumor necrosis factor-alpha, with beta-actin serving as a control. Gamma interferon mRNA, but not tumor necrosis factor alpha mRNA, was detectable in 4 of 5 psoriatic epidermal specimens. Neither mRNA was detectable in any normal skin dermal/epidermal specimens. Gamma interferon mRNA was also detectable in a single psoriatic dermal specimen. If reverse transcriptase was omitted, no polymerase chain reaction products were detected, indicating that the fragments detected were not derived from contaminating genomic DNA. These results indicate that gamma interferon mRNA can be extracted and successfully detected from human psoriatic lesional skin biopsies, using polymerase chain reaction technology. This molecular approach can easily be expanded to measure many other cytokines in both epidermal and dermal locations. The detection of gamma interferon in this clinical setting may be of particular pathophysiological significance because injection of gamma interferon has been reported to induce psoriatic lesions.

We describe a case of clear cell basal cell carcinoma of the superficial type, presenting as a crusted eruption on the abdomen. Histological examination showed a solid proliferation of clear cells attached to the under-surface of an atrophied epidermis. In addition, distinct pagetoid infiltration was seen within the overlying epidermis. A focal connection between the clear cell portion and a deeper lying nodular basal cell carcinoma was demonstrated, elucidating the true nature of the lesion. Immunohistochemical studies and electronmicroscopy confirmed the epithelial derivation of the tumour. The clear cell appearance was due to multiple cytoplasmic electronlucent vacuoles which were not surrounded by membranes.

We describe the case of a 38-year-old woman with adult-onset porokeratotic eccrine ostial and dermal duct nevus. The patient had a 9-year history of multiple keratotic papules and comedo-like pits on the medial border of the left foot. Light- and electron microscopic studies showed multiple cornoid lamella-like parakeratotic columns, which invariably were associated with hyperplastic eccrine ostia and distal sweat ducts. It is concluded that this entity, the first reported case of adult-onset porokeratotic eccrine ostial and dermal duct nevus, is a variant of the congenital form described previously by Abell and Read and by Aloi and Pippione.

The complete nucleotide sequence of 5-S RNA from Bacillus licheniformis was determined by analysis of complete and partial digests obtained with either T1 or pancreatic ribonuclease. The molecule was found to have a length of 116 nucleotides and may possess a minor sequence heterogeneity. There is a large degree of homology between the sequence of B. licheniformis 5-S RNA and those published for 5-S RNA from B. megatherium and B. stearothermophilus. The difference between the three 5-S RNA species are limited mainly to the two terminal and one internal sequence. B. licheniformis 5-S RNA contains the sequence U95-G-A-G-A-G100, which in B. subtilis has been implicated in the processing of precursor 5-S RNA. Possible models for the secondary structure of prokaryotic 5-S RNA are discussed on the basis of the results of limited digestion of B. licheniformis 5-S RNA by ribonuclease T1.