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A 62-year-old woman had multiple plasmacytomas in the skin and lymph nodes, without Bence-Jones protein or a monoclonal peak of serum immunoglobulins. Infiltrating plasmacytoid cells expressed cytoplasmic IgG (lambda) and surface CD38, without any B-cell markers. There was no visceral or bone marrow involvement suggestive of multiple myeloma. Southern blot analysis of extracted DNA from the cutaneous lesions showed two rearranged bands with an immunoglobulin, but not a T-cell receptor, gene probe. The patient showed a poor response to chemotherapy, and died of bronchopneumonia. The clinical course and cytological features differentiate multiple cutaneous extramedullary plasmacytomas from solitary cutaneous extramedullary plasmacytoma and cutaneous lesions associated with multiple myeloma.

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SUMMARYIn vitro FCERII expression was examined in patients with atopic dermatitis, those with non-atopic eczematous dermatitis and normal individuals following stimulation of peripheral blood cells with recombinant IL-4 (rIL-4), phytohaemagglutinin (PHA), or PHA plus rIL-2, At various days cells were stained with MoAbs to human lymphocyte FcsRII and to lymphoid cell-surface antigens and analysed by flow cytometry, rIL-4, but not rIL-2, specifically induced FCERII on T cells as well as B cells in atopic dermatitis, eczematous dermatitis and normal individual groups. Both atopies and non-atopies generated comparable proportions of FceRII"*" T cells (Ts cells), whereas the frequency of B cells bearing Fc£RII(B£ cells) was significantly higher in patients with extensive atopic dermatitis than in those with mild atopic dermatitis and other subjects. Comparable levels of Ts cells were detected in both atopic and non-atopic donors following stimulation of peripheral blood cells with PHA or pre-activation ofthe cells with PHA plus subsequent incubation with rIL-2, Whereas both CD8+ and CD4+ subsets were present in Te cell populations induced specifically by rIL-4, PHA and PHA plus rIL-2, patients with atopic dermatitis had a greater tendency for FCERII expression on 008"*" T cells compared with patients with eczematous dermatitis and normal individuals, Recombinant interferon-gamma (rIFN-y), but not rIFN-a or prostaglandin E2 (PGE2), suppressed the generation of TE cells by rIL-4 in atopies and non-atopies to the same degree. These results suggest the aberrant control of FCERII expression on T cells, especially those bearing CD8, in atopic dermatitis.