SummaryThe cytotoxic activity and pore-forming protein (PFP) expression of human peripheral blood (PB) y/S T cells were examined. Fresh y/S T cells isolated from PB lymphocytes by fluorescenceactivated cell sorting exhibited a substantial natural killer-like cytotoxic activity against K562 target cells and had a high cytotoxic potential triggered by anti-CD3 monoclonal antibody (mAb) against P815 target cells bearing FcyR. Immunocytochemical staining with an anti-PFP mAb revealed that virtually all PB y/S T cells are granular lymphocytes with abundant PFP in their cytoplasmic granules. Constitutive expression of PFP in PB 'y/6 T cells was also demonstrated by Northern blot analysis. These observations support the proposed role ofy/S T cells in cytolysic immune surveillance in vivo.

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Human interferon-gamma (IFN-gamma) is an important immunomodulatory protein produced predominantly by T cells and large granular lymphocytes (LGLs). Whereas large amounts of data have been accumulated regarding IFN gamma gene expression in these two cell types, little information about IFN gamma expression in other cell types exists. In this study, we have analyzed the production of IFN gamma by the Epstein- Barr virus (EBV)-positive B-cell line, JLP(c), derived from a patient with Burkitt's lymphoma, and another human B-cell line, PA682BM-1, which was derived from an acquired immunodeficiency syndrome patient. Southern blot analysis indicates the presence of an Ig heavy chain gene rearrangement, but no rearrangement of the T-cell receptor beta chain gene or IFN gamma gene in these B-cell lines. Both cell lines were found to express surface IgD and other B-cell surface markers, thus confirming their B-cell lineage. Analysis for surface Ig, cytoplasmic Ig, and secreted Ig indicates that the two cell lines are in relatively early stages of the B-cell differentiation pathway. We now report that PA682BM-1 can be triggered by the protein kinase C (PKC) activators, phorbol 12-myristate 13-acetate (PMA) and (-)Indolactam-v, to secrete IFN gamma, whereas JLP(c) cells spontaneously produce low levels of IFN gamma that can be enhanced by PKC activators and interleukin-2 (IL-2). After activation of the cell lines with IL-2, (-)Indolactam-v, and PMA, increases in cytoplasmic messenger RNAs (mRNAs) of IFN gamma and the IL- 2 receptor chains were also observed. The induction of IFN gamma mRNA and protein by IL-2 was completely blocked by a monoclonal antibody to IL-2 receptor p75 (beta chain), but not by the monoclonal antibody to p55 (alpha chain). Analysis of IFN gamma genomic DNA indicates that the gene is not amplified, but that hypomethylation in the 5′ noncoding region of the IFN gamma gene has occurred in the B-cell line from the Burkitt's lymphoma patient that spontaneously produces IFN gamma. This finding suggests that the methylation state of the promoter region may play an important role in the control of IFN gamma gene expression in B cells.

A 68-year-old male with Paget's disease of the esophagus is reported. The underlying primary esophageal carcinoma was diagnosed as adenosquamous cell carcinoma on the basis of the presence of both adenocarcinoma and epidermoid carcinoma components. There was invasive growth of clear Paget's cells in the esophageal epithelium. Much histochemistry disclosed common characteristics of mucin between Paget's cells and adenosquamous cell carcinoma. It was histochemically confirmed that the existence of much was a general feature of extramammary Paget's disease. In 13 control esophageal carcinomas including three with adenocarcinomatous elements, Paget's cells were not found in the epithelium. To date only one case of Paget's disease of the esophagus has been described in the literature. ACTA PATHOL J P N 38: 651-658, 1988.