Identification of tissue transglutaminase as the autoantigen of celiac disease

@article{Dieterich1997IdentificationOT,
  title={Identification of tissue transglutaminase as the autoantigen of celiac disease},
  author={Walburga Dieterich and Tobias Ehnis and Michael Bauer and Peter Donner and Umberto Volta and Ernst Otto Riecken and Detlef Schuppan},
  journal={Nature Medicine},
  year={1997},
  volume={3},
  pages={797-801}
}
Celiac disease is characterized by small intestinal damage with loss of absorptive villi and hyperplasia of the crypts, typically leading to malabsorption1. In addition to nutrient deficiencies, prolonged celiac disease is associated with an increased risk for malignancy, especially intestinal T-cell lymphoma1–3. Celiac disease is precipitated by ingestion of the protein gliadin, a component of wheat gluten, and usually resolves on its withdrawal. Gliadin initiates mucosal damage which involves… Expand
Transglutaminase 2 and Transglutaminase 2 Autoantibodies in Celiac Disease: a Review
TLDR
The role of TG2, TG2-specific B cells, and autoantibodies in celiac disease is assessed and blocking the enzymatic activity ofTG2 has been suggested as a suitable novel pharmacological approach to treat Celiac disease. Expand
The function of tissue transglutaminase in celiac disease.
TLDR
This review is focused on the function of tTG in celiac disease, although it also deals with novel advances in tTG-based therapies. Expand
Tissue transglutaminase--the key player in celiac disease: a review.
TLDR
TTG can be used as the first line diagnostic test in the work-up of celiac disease, as well as for screening purposes and may contribute to future strategies in treating Celiac disease either by producing nontoxic wheat or by generating oral vaccination that can prevent the disease. Expand
Immunoassay for detection of IgA antitissue transglutaminase in patients with celiac disease.
TLDR
Serum IgA antibodies against endomysial antibodies are especially considered to be sensitive and highly specific markers for celiac disease, and were detected by indirect immunofluorescence on tissue slides of monkey esophagus or human umbilical cord. Expand
Gluten in infants and celiac disease risk
TLDR
There is no evidence to give specific recommendations for the age of gluten introduction or breast-feeding to prevent celiac disease, and it was endorsed that, in order to induce tolerance, gluten should be initiated gradually at the ageof 4–6 months, preferably during ongoing breastfeeding. Expand
Tissue transglutaminase in celiac disease: role of autoantibodies
TLDR
A brief summary of anti-tTG antibody effects demonstrating that these antibodies are functional and not mere bystanders in the disease pathogenesis is reported. Expand
Pathomechanisms in celiac disease.
TLDR
Modification of gluten peptides by tTG can enhance their binding to HLA-DQ2 or -DQ8 and potentiate T cell stimulation, and tTG-catalyzed cross-linking and consequent haptenization of gluten with extracellular matrix proteins allows for storage and extended availability of gluten in the mucosa. Expand
Pathomechanisms in Celiac Disease
TLDR
Modification of gluten peptides by tTG can enhance their binding to HLA-DQ2 or -DQ8 and potentiate T cell stimulation, and tTG-catalyzed cross-linking and consequent haptenization of gluten with extracellular matrix proteins allows for storage and extended availability of gluten in the mucosa. Expand
Mucosal tissue transglutaminase expression in celiac disease
TLDR
Overall, it is found that tTG is equally expressed in CD at different stages of disease; and assessment of tTG level in biopsy samples by immunohistochemical methods is not useful in the clinical diagnostic work‐up of CD. Expand
Recent developments in the pathogenesis, diagnosis and treatment of celiac disease
TLDR
Three patents from the last four years are reviewed, related to the antigenic role of tissue transglutaminase, the immunodominant gliadin peptide recognised by the cells in the peripheral blood of individuals with CD and the pro-inflammatory role of IL-15. Expand
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 36 REFERENCES
Production of antiendomysial antibodies after in-vitro gliadin challenge of small intestine biopsy samples from patients with coeliac disease
TLDR
The results suggest that a more complex pathogenetic mechanism than normally accepted is involved in coeliac disease and raise the possibility that EMA, or the antigen recognised by them, are involved directly in the pathogenesis of CD. Expand
Wheat peptide challenge in coeliac disease
TLDR
The results suggest that the oligopeptide corresponding to aminoacids 31-49 of A-gliadin is toxic in vivo, but there is no evidence of toxicity of the far N-terminal peptide, residues 3-21, which may contain an epitope to which patients with coeliac disease display variable sensitivity. Expand
Gluten, major histocompatibility complex, and the small intestine. A molecular and immunobiologic approach to the spectrum of gluten sensitivity ('celiac sprue').
  • M. Marsh
  • Biology, Medicine
  • Gastroenterology
  • 1992
TLDR
The nature and basis of nonresponsive celiac sprue require more thoughtful initiatives to elucidate the immunologic mechanism(s) of unresponsiveness and evaluate possible means of reversal. Expand
Human jejunal transglutaminase: demonstration of activity, enzyme kinetics and substrate specificity with special relation to gliadin and coeliac disease.
TLDR
It is postulated that intestinal transglutaminase activity may be important in gliadin binding to tissues and thus in the pathogenesis of coeliac disease. Expand
Antigliadin and antiendomysium antibody determination for coeliac disease.
TLDR
Patients who are young at diagnosis of coeliac disease and without a morphological relapse were less than 2 years old at diagnosis so it is concluded that patients who areYoung at diagnosis should be challenged. Expand
Coeliac disease in the year 2000: exploring the iceberg
TLDR
Screening in a school district in central Italy can detect large numbers of cases of coeliac disease, which can be treated with a gluten-free diet and would not be detected by screening only a selected group of at-risk patients. Expand
Endomysium antibodies in coeliac disease: an improved method.
TLDR
The easy availability and enhanced testing sensitivity of the umbilical cord is an advance towards a better diagnostic tool for coeliac disease. Expand
Malignancy in coeliac disease--effect of a gluten free diet.
TLDR
The results indicate that for coeliac patients who have taken a GFD for five years or more the risk of developing cancer over all sites is not increased when compared with the general population, and give further support for advising all patients to adhere to a strict G FD for life. Expand
Immunological diagnosis of childhood coeliac disease: comparison between antigliadin, antireticulin and antiendomysial antibodies
TLDR
Compared with AGA and ARA sensitivity, specificity and predictive values, EMA is the most reliable serological marker for the diagnosis of coeliac disease and should be considered the best of the three serological tests available for childhood coeliasis. Expand
Gliadin-specific, HLA-DQ(alpha 1*0501,beta 1*0201) restricted T cells isolated from the small intestinal mucosa of celiac disease patients
TLDR
The findings suggest preferential mucosal presentation of gluten-derived peptides by HLA-DQ(alpha 1*0501, beta 1*0201) in CD, which may explain the HLA association. Expand
...
1
2
3
4
...