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A proportion of epithelial lymphocytes in various mammalian species is characterised by cells containing cytoplasmic granules. We have studied the total number of granular lymphocytes within surface and crypt epithelium of jejunal mucosae (per 104 µm2 muscularis mucosae) from six groups of subjects, comprising (i) young healthy volunteers (ii) family relatives of known coeliac patients, patients with gastrointestinal disorders associated with either (iii) normal or (iv) “flat” mucosae, and groups of (v) untreated and (vi) treated patients with coeliac disease. There was no difference in the absolute number of gEL between the three control groups with normal mucosal architecture, the proportion of granular to total EL per unit of tissue varying between 30–40% . In untreated coeliac mucosae, there was a significantly increased population of gEL, compared with the same control groups (p<0.001): the ratio of granular to total EL approximated 65%, and did not differ from flat-control mucosae in which the proportion of gEL was 55%. On withdrawal of gluten, the absolute number of gEL fell significantly in comparison with the untreated coeliac group (p< 0.05). To further evaluate the effect of gluten challenge, granular lymphocytes were monitored during a five-day period in groups of treated coeliac patients orally challenged with increasing doses (500–3000 mg) of a peptic-tryptic digest of gluten. A significant rise in the absolute number of granular lymphocytes occurred at 12 h, but without any deterioration in mucosal architecture.

Sturgess RP, Loft D, Kontakou M, Crowe P, Marsh MN, Ciclitira PJ. Rectal epithelial γ/δ T-lymphocyte responses to local gluten challenge in coeliac disease. Scand J Gastroenterol 1993;28:760-762.The proportion of intra-epithelial lymphocytes (IEL) that utilize the γ/δ form of the T-cell receptor (TCR) is increased in coeliac disease, but their function remains unexplained. The response of intraepithelial lymphocytes to rectal gluten challenge in coeliac and control subjects was studied after a rectal challenge of 2 g of Frazer's fraction III. A marked rise in CD3+ IEL occurred after challenge in the coeliac patients, peaking at 6 h and returning to normal by 48 h, with no significant changes in the γ/δ TCR+ IEL. The IEL did not significantly change after gluten challenge in the controls. Acute gluten challenge induces infiltration of the rectal mucosa by T cells in coeliac patients, which is not accompanied acutely by increased numbers of γ/δ TCR+ IEL. This study supports the hypothesis that α/β TCR+ T cells may be of importance in the early response of coeliac patients to local gluten challenge.

One hundred and sixty-two of 182 patients with coeliac disease provided satisfactory details of family size and the prevalence of coeliac disease and inflammatory bowel disease among their first-degree relatives. Patients ranged in age from 11 months to 79 years with a mean age of 41 (± 23) years. Twenty patients had at least one first-degree relative with coeliac disease: a total of 25 of 861 relatives were affected (prevalence=2904/100,000) compared with an expected 0.9 cases (prevalence=100/100,000; p <0.001). Six relatives had inflammatory bowel disease (prevalence=697/100,000) compared with an expected 1.3 cases (prevalence=150/100,000; p <0.001). Five of these had ulcerative colitis, and one had Crohn's disease. The relative risk of ulcerative colitis is, therefore, five times greater for first-degree relatives of people with coeliac disease than for the general population (95 per cent confidence interval, 4.7–7.2). There is clear association between coeliac disease and ulcerative colitis, which may point to factors involved in the aetiology of colitis.