SUMMARY Immunohistological techniques using monoclonal antibodies were employed to study the morphology and phenotypic expression of macrophage like cells in ulcerative colitis, Crohn's colitis and histologically normal colonic mucosa. The antibody RFD1 identifies interdigitating (antigen presenting) cells whereas RFD7 binds to mature tissue macrophages. In normal colonic mucosa, the majority of cells recognised by these reagents were positive for Class II antigen expression and a median 87% (range 80-95%) were positive for both RFD1 and RFD7, with 6.5% (ranges 1-14%) positive for either antibody alone. There was much greater macrophage heterogeneity in the ulcerative colitis and Crohn's colitis biopsies than in normal mucosa. Clusters of RFD9+ cells (epithelioid cells) were found in Crohn's colitis and, to a lesser extent, in ulcerative colitis. Some Crohn's colitis sections showed replacement of the normal colonic macrophage phenotype with RFD1-RFD7+ cells (classical scavenger macrophages). The degree of this replacement correlated with the histological severity ofthe disease. By contrast, large numbers of RFD1+ RFD7-cells, with long dendritic processes, were found in intimate association with the lymphoid infiltrates in the lamina propria of the ulcerative colitis sections. Future studies of the factors controlling macrophage differentiation in tissues may help to explain the greater macrophage heterogeneity in inflammatory bowel disease and the differences between ulcerative colitis and Crohn's colitis observed in this study.It is probable that non-lymphoid mononuclear cells

The Th2 cytokines, interleukin (IL)-4 and IL-5, have an important role in atopic disease. CD30 is a transmembrane molecule that may be expressed on a proportion of activated T-lymphocytes and has been reported to be a marker for Th2 phenotype. Our objective was to compare the in vitro cytokine responses and CD30 expression of peripheral blood mononuclear cells (PBMCs) to stimulation with house dust mite antigen (Dermatophagoides pteronyssinus) in atopic asthmatics, atopic nonasthmatics, and normal subjects, and to see if atopic asthmatic cytokine production correlated with symptomatic disease activity and whether cytokine production was allergen-specific. Eighteen atopic asthmatics (all were allocated a symptomatic disease score), 6 atopic nonasthmatics, and 7 healthy nonatopic individuals were studied. Resting serum IL-4 levels were measured, then PBMCs were separated using Lymphoprep density centrifugation and cultured in modified RPMI 1640 medium. PBMCs were stimulated with IL-2 alone or with D. pteronyssinus (1,000 subcutaneous units/ml) with IL-2 and harvested after 5 and 10 d. Using monoclonal antibodies and flow cytometry we obtained the percentage of CD4+ T cells expressing CD30 and the intensity of CD30 staining. Culture supernatants were analyzed for IL-4 and interferon gamma (IFN-gamma) using an enzyme-linked immunosorbent assay. In 9 atopic asthmatics PBMCs were also stimulated nonspecifically using phytohemagglutinin (PHA). IL-4 was detectable in the serum of atopic subjects but not in normal subjects. Stimulation of PBMCs with D. pteronyssinus produced significant amounts of IL-4 in atopic asthmatics and atopic nonasthmatics, but minimal quantities in normal subjects. Much lower levels of IFN-gamma were produced by atopic asthmatics in response to D. pteronyssinus compared to atopic nonasthmatics. IFN-gamma levels had an inverse correlation with asthmatic symptom score. CD4+ T-cell expression of CD30 also correlated inversely with IFN-gamma production and IFN-gamma:IL-4 ratio. PHA produced minimal levels of IL-4 compared to specific allergen stimulation. It is concluded that different groups of atopic patients exhibit different patterns of allergen-induced cytokine production. In vitro allergen-induced cytokine production in atopic asthmatics correlated with symptomatic disease activity, and is allergen-specific.

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Immunohistological analysis of bronchial biopsy specimens from nine patients with bronchiectasis and four control subjects was performed with a panel of monoclonal antibodies selected to show lymphocyte and macrophage subsets and signs ofcellular activation. The cells taking part in the inflammatory response in the bronchial wall of patients with bronchiectasis were almost exclusively mononuclear cells, most of them T lymphocytes. B lymphocytes were observed in biopsy specimens from only two out ofnine patients. CD8+ T cells outnumbered CD4+ cells in all patients in a ratio ranging from 2:1 to 10:1. Most T lymphocytes also strongly expressed CD7 antigen and a proportion of them expressed HLA-DR. Most of the lymphocytic infiltration occurred just beneath the basement membrane of the epithelium, though intraepithelial and submucosal infiltration was also seen. Non-lymphoid mononuclear cells expressing the phenotype of dendritic cells and macrophages were found dispersed throughout the infiltrate, most of them expressing HLA-DR. These observations support the hypothesis that cell mediated immunological reactions contribute to the inflammation associated with bronchiectasis.