The distribution of IgA1- and IgA2-containing cells was studied in 27 normal specimens taken from 3 parts of the intestine: the upper jejunum (8), the terminal ileum (5), and the large bowel (14). IgA1- and IgA2-containing cells were identified by an immunoperoxidase staining using mouse anti-IgA1 or IgA2 monoclonal antibody. The sum of IgA1-containing cells (IgA1+) and IgA2-containing cells (IgA2+) was greatest in the large bowel and least in the terminal ileum. IgA1+ were most frequent in the jejunum and least in the terminal ileum while IgA2+ were most frequent in the large bowel and least in the jejunum (p less than 0.005). The ratio of IgA1+/IgA2+ was 1.63 +/- 0.41 in the jejunum which was significantly higher than 0.65 +/- 0.46 in the terminal ileum (p less than 0.05) and 0.63 +/- 0.2 in the large bowel (p less than 0.001). These results lead to the new recognition that there is a shift in preponderance of IgA subclasses in the intestine, namely IgA1+ cells predominate in the jejunum and IgA2+ cells predominate in the intestine distal to the terminal ileum.

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Spontaneous cell-mediated cytotoxicity (SCMC) and the marker of natural killer (NK) cells mediating SCMC of the human large intestine were studied. Lamina proprial lymphoid cells (LPL) were isolated by sequential dithiothreitol-EDTA-collagenase treatment of the gut specimen. SCMC was measured by the chromium release method. Target cells included P4788 in monolayer, a cell line derived from colon cancer, Chang cells in monolayer, and K562 in suspension. Target cells in monolayer including colon cancer cell line were chosen because they were thought to be more appropriate to assess SCMC for lymphoid cells in the solid organ. While lower compared to cytotoxicities (CT) by peripheral blood lymphoid cells (PBL), define CT were observed in LPL against all three targets. NK cells marker was studied both on LPL by an indirect fluorescent antibody method and on the gut tissue by indirect immunoperoxidase staining using anti HNK-1 monoclonal antibody which defines virtually all NK cells. HNK-1 positive (HNK-1 +) cells were identified in both methods. HNK-1 + cells were observed in the epithelium, lamina propria, and lymph follicle with or without germinal centers. These results clearly demonstrated the presence of SCMC and HNK-1 + cells in the human large bowel.

Although the expression of HLA-DR antigens on colonic epithelium in ulcerative colitis has been observed by several groups, the results of the expression in remission have been conflicting and there has been virtually no study concerning the expression in non-inflamed area in active ulcerative colitis. We studied systematically HLA-DR expression on colonic epithelium in 37 patients with ulcerative colitis chronologically, namely in remission as well as in the active stage and inflamed and non-inflamed areas simultaneously in the active stage. HLA-DR antigens were detected by indirect peroxidase staining using anti-HLA-DR monoclonal antibody. We confirmed the previous observation that epithelium from control colon does not express HLA-DR antigens, while epithelium from ulcerative colitis expresses the antigens with high frequency (83.3 percent). In addition, we demonstrated that HLA-DR expression on colonic epithelium in active ulcerative colitis disappeared in remission. Our new finding was that there is no HLA-DR expression on colonic epithelium in non-inflamed mucosa in active ulcerative colitis. Namely HLA-DR antigens were expressed only on inflamed epithelium of ulcerative colitis. These results lead to the conclusion that the expression of HLA-DR antigens on colonic epithelium in ulcerative colitis is closely related to the inflammation of mucosa.

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