Transcription of the adenovirus type 2 peptide IX (pIX) gene was examined in transient expression assays. When a nonreplicating plasmid DNA containing the pIX gene was introduced into HeLa cells by the DEAE-dextran method, no pIX gene transcript was detected. In contrast, efficient transcription was observed in the cells transfected with a replicating plasmid containing the pIX gene. Adenovirus early genes did not affect the level of transcription of the pIX gene on either a nonreplicating or a replicating plasmid. Inhibition of plasmid replication with cytosine arabinoside prevented transcription of the pIX gene. By quantitative analysis of the amount of the pIX gene and its transcript in transfected cells, it was concluded that active transcription of the pIX gene occurred only on DNA molecules replicated in the cell.

We investigated the effects of the antibodies against the adhesion molecules leucocyte function associated antigen-1 (LFA-1) and intercellular adhesion molecule-1 (ICAM-1) on mouse allergic contact hypersensitivity. Mice were injected intraperitoneally with both antibodies before sensitization by an epicutaneous application of dinitrofluorobenzene (DNFB). Simultaneous administration of the antibodies induced suppression of ear swelling in the effector phase of contact hypersensitivity. To show the effect of antibodies in vitro, lymph node cells (LNC) of mice treated with antibodies or with phosphate-buffered saline (PBS) were cultured in the presence of dinitrobenzene sulphonic sodium salts (DNBS), and the production of interleukin-2, interleukin-4 and interleukin-10 in the culture supernatants was measured using an enzyme-linked immunosorbent assay (ELISA). It was found that the production of interleukin-2 in the cells of mice treated with the antibodies was significantly lower than in the cells of PBS-treated mice. On the other hand, no difference was noted in the production of interleukin-4 or interleukin-10. Our results indicate that in vivo simultaneous administration of antibodies to cell adhesion molecules before hapten sensitization induces the suppression of contact hypersensitivity in mice and that the suppression may be due to the inhibition of the production of interleukin-2.

We report an 85-year-old man with squamous cell carcinoma on the right pinna. Two years after the excision of the lesion, metastatic foci were found extending from the right retromandibular to the mastoid region and into the parapharyngeal space. Histopathologically, the primary tumor showed interconnecting nests of atypical cells invading into the dermis from multiple epidermal and infundibular foci. The tumor had both squamous and glandular differentiation. A peculiar finding was the presence of decapitation secretion in the glandular foci. To our knowledge, definite apocrine differentiation in squamous cell carcinoma has not previously been reported.

Isologous free skin grafts were applied to the backs of BALB/c mice and contact hypersensitivity studied by epicutaneous application of DNFB (2,4-dinitro-1-fluorobenzene) to the grafted skin. In the first experiment, the grafted skin was sensitised and the elicitation reaction assessed by measuring the ear swelling after five days. Sensitisation was not successful until two weeks after grafting. In such non-responding animals, re-sensitisation with DNFB on the ungrafted skin area was also unsuccessful, indicating the establishment of immunological tolerance. This tolerance was considered antigen-specific, as re-sensitisation with oxazolone was successful. In the second experiment, spleen cell suspension, both untreated and treated in vitro with antiThy 1.2, antiLyt 1.2, and antiLyt 2.2 antibody, from non-DNFB-responding mice was transferred into normal mice. Subsequently these mice were sensitised with DNFB. Sensitisation was not successful in the untreated group or in those treated with antiLyt 1.2 antibody. On the other hand, the groups treated with antiThy 1.2 and antiLyt 2.2 antibody did become sensitised. These results indicate that the unsuccessful delayed hypersensitivity of the grafted skin was caused by suppressor T cells. In addition, the density of epidermal Langerhans cells was reduced in the early stages of skin grafting and morphological abnormalities were present. From these results, we conclude that contact sensitisation during the early stage of grafting skin not only produces suppression of ear swelling but also induces antigen-specific tolerance. These results also suggest that the suppression depends on the antigen-specific suppressor cells and that acquirement of tolerance is associated with a reduction in the number of epidermal Langerhans cells in the grafted skin and abnormalities in their structure.

Transcription of the adenovirus type 2 peptide IX (pIX) gene was examined in transient expression assays. When a nonreplicating plasmid DNA containing the pIX gene was introduced into HeLa cells by the DEAE-dextran method, no pIX gene transcript was detected. In contrast, efficient transcription was observed in the cells transfected with a replicating plasmid containing the pIX gene. Adenovirus early genes did not affect the level of transcription of the pIX gene on either a nonreplicating or a replicating plasmid. Inhibition of plasmid replication with cytosine arabinoside prevented transcription of the pIX gene. By quantitative analysis of the amount of the pIX gene and its transcript in transfected cells, it was concluded that active transcription of the pIX gene occurred only on DNA molecules replicated in the cell.