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SUMMARY Complement activation may play an important role in the pathogenesis of coeliac disease. In the present study immunohistochemical localisation of C3 and of a neoantigen exposed only on the terminal C5b-9 complement complex has been performed on small intestinal biopsy sections from newly diagnosed untreated coeliac patients, from coeliac patients on long-term glutenfree diet and from disease controls. Levels of C3 were markedly increased in treated coeliac patients compared with controls. Staining of C3 was concentrated subepithelially and within the centre of the lamina propria. No staining was detected at these sites using antibody to the neoantigen, however, strongly suggesting that the increased levels of C3 seen in the coeliac patients was the result of increased extravasation of serum proteins rather than complement activation. Surprisingly, complement activation was detected within the glands of Brunner. Positive staining using anti-C5b-9 neoantigen was found in all coeliac patients, both treated and untreated.

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Serum IgA anti-gliadin antibody estimation is a recognized screening method for celiac disease. However, celiac disease is primarily a small intestinal mucosal disorder, and so we have examined the possibility that secreted, mucosal IgA anti-gliadin antibody might provide a more relevant measure of gluten sensitivity than that obtained from serum tests. Serum IgA anti-gliadin antibody and serum, salivary, and small intestinal aspirate IgA anti-gliadin antibody were measured by enzyme-linked immunosorbent assay. Serum IgA and IgG anti-gliadin antibody were markedly increased in untreated celiacs (N = 31) as compared to normals (N = 20) or disease controls (N = 39) (P less than 0.0001). Levels were lower in treated (N = 30) than untreated celiacs (P less than 0.001). In intestinal aspirates both untreated and treated patients had similar levels of IgA anti-gliadin antibody (P = 0.48), but both were significantly higher than in controls (P less than 0.01). Salivary IgA anti-gliadin antibody, by contrast, was not increased in celiac patients as compared to controls. Serum IgA anti-gliadin antibody was the most sensitive (84%) and specific (95%) test for detecting untreated celiac disease. It was also the most useful in patient follow-up where it provides an early objective indicator of adherence to a gluten-free diet. Mucosal IgA responses to gliadin in celiac disease appear to be compartmentalized, with different portions of the gastrointestinal tract functioning as separate immunological organs. Our results also demonstrate that serum and secretory IgA production are under independent control.

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