Circulating antibodies to wheat gliadin fractions in coeliac disease

Cornell, Hugh J.

doi:10.1136/adc.49.6.454

Cited by 18 publications

(10 citation statements)

References 24 publications

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“…In line with this, serologic testing for celiac disease specific antibodies is an increasingly important tool in the diagnostic workup of patients. The first serologic tests were developed 50 years ago based on anti-gliadin antibodies binding to native gliadin antigen [49,50], but these tests show relatively poor sensitivity and specificity. It was later discovered that celiac disease patients have autoantibodies to reticular fibers of connective tissue [51].…”

Section: Antibody Response In Celiac Diseasementioning

confidence: 99%

T-cell and B-cell immunity in celiac disease

Pré

Sollid

2015

Best Practice & Research Clinical Gastroenterology

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Section: Antibody Response In Celiac Diseasementioning

confidence: 99%

T-cell and B-cell immunity in celiac disease

Pré

Sollid

2015

Best Practice & Research Clinical Gastroenterology

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“…Patients with coeliac disease (CD) usually have substantial levels of serum antibodies to gluten [2,7,10,11,15]; this activity is mainly expressed by the IgG isotype [1,4,14]. Fairly high levels of such antibodies may be present also in patients with other intestinal disorders and in normal subjects [4,6].…”

Section: Introductionmentioning

confidence: 99%

Changes of Serum Antibody Activities to Various Dietary Antigens Related to Gluten Withdrawal or Challenge in Children with Coeliac Disease

Scott¹,

J²,

Brandtzæg³

1985

Int Arch Allergy Immunol

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IgG, IgA, and IgM serum antibody activities to gluten, a gluten fraction called glyc-gli, and antigens from egg and cow’s milk were monitored by an enzyme-linked immunosorbent assay (ELISA) in children with coeliac disease during treatment and gluten challenge. The IgA activity to gluten antigens showed in most patients a rapid and significant reduction after gluten withdrawal, whereas the IgG activity decreased more slowly. During gluten challenge, both these activities rose significantly, and the increases could usually be detected several months before overt clinical relapse. Such determinations, therefore, represent a valuable adjunct in the follow-up of children with coeliac disease. IgA activities to egg and cow’s milk antigens likewise tended to decrease after gluten withdrawal and increase during challenge, but the changes were less consistent for individual antigens. Nevertheless, monitoring of IgA activities to a selection of dietary antigens other than gluten may be particularly valuable when it comes to evaluation of intestinal responses in patients on a glutenfree diet.

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“…Secondly, by means of the purified fractions employed, it has now been demonstrated, in a direct manner, that some of the relatives of coeliac patients have a partial deficiency in their ability to digest these fractions. Indirectly, an abnormality had already been indicated (Cornell, 1974). Thus, in some of these relatives, there appear to be mucosal biochemical features which have more in common with remission coeliac mucosa than with normal control mucosa.…”

Section: Discussionmentioning

confidence: 97%

Further evidence of a primary mucosal defect in coeliac disease: In vitro mucosal digestion studies in coeliac patients in remission, their relatives, and control subjects

Cornell¹,

Rolles²

1978

Gut

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SUMMARY Subfractions of fraction 9, obtained from a peptic-tryptic-pancreatinic digest of wheat gliadin, were subjected to in vitro mucosal digestion and the filtrates examined for residual peptides. Small-intestinal mucosa from four groups of individuals were studied-eight patients with coeliac disease in remission; eight healthy controls; nine first degree relatives of patients with coeliac disease, and six children with recurrent diarrhoea investigated for possible coeliac disease, but in whom the diagnosis was excluded. The highest amounts of residual peptides (measured by scanning densitometer) were detected after digestion with mucosa from patients with coeliac disease and the lowest amounts with the control groups. The results obtained with the group of relatives fell between those of the coeliac disease and control groups, while the recurrent diarrhoea group overlapped the relatives and controls. The residual peptides were derived chiefly from the B-type subfractions of subfractions 1 and 2, obtained by ion-exchange chromatography of fraction 9. These subfractions are rich in glutamine/glutamic acid and proline and have a molecular weight (apparent) of not greater than 1500 Daltons. The results lend further support to the hypothesis of an enzyme deficiency in coeliac disease. A partial enzyme deficiency may exist in some first-degree relatives and in some children with recurrent diarrhoea but with histology of the small intestine within normal limits. HLA-B8 antigen is not correlated with this deficiency, but, when the two factors are associated, they could be related to the manifestation and severity of coeliac disease.The demonstration that an ultrafiltrate of a peptictryptic-pancreatinic digest of wheat gliadin was toxic to patients with coeliac disease (Bronstein et al., 1966) has led to mucosal digestion studies in vitro on fractions of this digest in an attempt to define the toxic substances (Cornell and Townley, 1973a). These latter studies have pointed to the possibility of an enzyme deficiency in the small intestine of patients with coeliac disease and this is linked to evidence that fraction 9 of this digest contains a large proportion of the toxic components of gluten. This is supported by the results of similar experiments with rye gliadin and by the ability of fraction 9 to cause significant reduction in D-xylose absorption in coeliac patients in remission (Cornell and Townley, 1974). Organ culture of small intestinal mucosa "Present address and address for reprints: Royal Melbourne

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Circulating antibodies to wheat gliadin fractions in coeliac disease

Cited by 18 publications

References 24 publications

T-cell and B-cell immunity in celiac disease

T-cell and B-cell immunity in celiac disease

Changes of Serum Antibody Activities to Various Dietary Antigens Related to Gluten Withdrawal or Challenge in Children with Coeliac Disease

Further evidence of a primary mucosal defect in coeliac disease: In vitro mucosal digestion studies in coeliac patients in remission, their relatives, and control subjects

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