Immune Response to Gluten in Adult Coeliac Disease

Housley, J.; Asquith, P.; Cooke, W. T.

doi:10.1136/bmj.2.5650.159

Cited by 37 publications

(10 citation statements)

References 11 publications

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“…This is indicated by the small spleen that may be found in adult coeliac disease and by the signs of splenic atrophy which are recognised in the blood, the presence of Howell-Jolly bodies being particularly striking. McCarthy et al (1966) have shown that there is a reduction in periph eral lymphoid tissue and it has also been shown that the lymphocytes in coeliac patients may show impaired transformation, whether they be circulating lym phocytes (Blecher et al, 1969) or lymphocytes teased out from mesenteric lymph nodes (Housley et al, 1969). All these findings suggest lymphoreticular dysfunction and this is supported by studies of the immunoglobulins in coeliac disease (Hobbs and Hepner, 1968) which have shown reduced levels of IgM in 60% of untreated patients.…”

Section: Immunological Abnormalities In Coeliac Diseasesupporting

confidence: 71%

Coeliac Disease

Booth¹

1977

Ann Nutr Metab

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In coeliac disease there is an abnormality of the intestinal mucosa which is caused by ingesting gluten. The intestinal lesion affects predominantly the proximal small intestine and the ileum is either normal or less severely involved than the jejunum. In some cases adaptive changes occur in the ileum, producing enhanced absorption in that region when there is malabsorption in the jejunum. The characteristic absorptive abnormality in coeliac disease is therefore jejunal malabsorption and Heal hyperabsorption. When such a situation develops it is possible that an individual with a flat jejunal mucosa may develop no symptoms of the disease, since the adaptive changes in the ileum compensate for the jejunal lesion. This may explain why in Western society there are probably more cases of coeliac disease undiagnosed in the community than have been treated by their doctors. The basic lesion in coeliac disease appears to be genetically determined and it is likely to be a failure to clear antigen which normally enters the lamina propria of the gut resulting in the formation of immune complexes with complement fixation at gut level.

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Section: Immunological Abnormalities In Coeliac Diseasesupporting

confidence: 71%

Coeliac Disease

Booth¹

1977

Ann Nutr Metab

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“…in the past, activation of lymphocytes by gluten fraction 111 has given variable results, for example, peripheral blood lymphocytes proliferate poorly in response to gluten fraction III, whereas mesenteric lymph node cells proliferate strongly after incubation with this antigen (8). Gluten fraction 111 is a peptic/tryptic digest of gluten, which is known to be toxic to the coeliac epithelium, and has been demonstrated to induce migration inhibition of leucocytes from coeliac subjects, but not from normal subjects (2,3.18).…”

Section: Discussionmentioning

confidence: 99%

Lymphocyte activation as measured by interleukin‐2 receptor expression to gluten fraction 111 in coeliac disease

Penttila

Gibson

Forrest

et al. 1990

Immunology & Cell Biology

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Summary Lymphocyte activation was examined by interIeukin-2 (IL-2) receptor expression on peripheral blood mononuciear cells from coeliac and control subjects. Purified T cells were incubated with gluten fraction 111 (a known toxic peptidc for coeliac subjects), soyabean hydrolysate (an unrelated hydrolysed food antigen), and Concanavalin-A (Con-A. a non-specific mitogen). After 1-5 days incubation, expression of IL-2 receptors was assessed using a cellular enzyme-linked immunosorbent assay (ELISA). Gluten fraction 111 induced expression of IL-2 receptors on T lymphocytes from coeliac but not ftom normal subjects (P^ 00005). whereas soyabean hydrolysate did not induce IL-2 receptor expression. Lymphocytes from both coetiac and normal subjects had similar increased IL-2 receptor expression after incubation with Con-A. Flowcytometry was also used to contirm specific expression of IL-2 receptor expression of lymphocytes from coeliac subjects. Interlcukin-2 receptor expression increased from 0 to 5-4% of cultured mononuclear cells after 7 days incubation with gluten fraction III. These cells were CD3-positiveand CD4-positivc. We conclude that peripheral blood lymphocytes from coeliac subjects are sensitized specifically to gluten fraction III.

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“…Impaired lymphocyte responsiveness to PHA has been demonstrated in coeliac disease (1,14,15) and an increase in the proportion of Ig-bearing (B) cells in the peripheral blood have been described (24). On a more general basis, an increased enteric loss of lymphocytes may explain the lymphoreticular dysfunction in this condition (21) and lymphopaenia has been reported as a feature of coeliac disease (3).…”

Section: Discussionmentioning

confidence: 99%

The Distribution and Enteric Loss of <sup>51</sup>Cr-Labelled Lymphocytes in Normal Subjects and in Patients with Coeliac Disease and Other Disorders of the Small Intestine

Douglas

Weetman

Haggith³

1976

Digestion

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Peripherally harvested lymphocytes have been labelled with ⁵¹Cr, reinjected into human subjects and their distribution then studied. Evidence is presented which suggests faecal loss of ⁵¹Cr represents loss of T lymphocytes and that there is normally a pathway of lymphocyte removal into the gut of probable importance in lymphocyte migration streams. In 9 normal subjects, without structural intestinal disease, faecal loss of lymphocytes over 5 days was 0.20 % (SEM ± 0.06) whereas in 5 patients with untreated coeliac disease faecal loss was 1.13 ± 0.34 %, in 7 with Crohn’s disease it was 1.01 ± 0.21 % and in 5 with intestinal lymphangiectasia loss was 0.61 ± 0.10%. In 1 patient with acute tropical sprue, enteric loss was 0.97 %. By contrast, faecal loss was normal in 3 coeliac patients in remission on a gluten-free diet. Measurements were also made using an external counter. In contrast to the normals, where count rates steadily diminished, an increasing activity was recorded over the umbilicus over 7 days after dose administration in all the disease categories studied with the exception of the treated coeliacs. The finding of an increased enteric loss of lymphocytes may explain many of the immunological abnormalities in the conditions studied.

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Immune Response to Gluten in Adult Coeliac Disease

Cited by 37 publications

References 11 publications

Coeliac Disease

Coeliac Disease

Lymphocyte activation as measured by interleukin‐2 receptor expression to gluten fraction 111 in coeliac disease

The Distribution and Enteric Loss of <sup>51</sup>Cr-Labelled Lymphocytes in Normal Subjects and in Patients with Coeliac Disease and Other Disorders of the Small Intestine

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