Celiac disease pathogenesis: The plot thickens

Gastroenterology

Volumn 123, Issue 3, 2002, Pages 939-943

  Kagnoff, Martin F ^a  

^a UNIVERSITY OF CALIFORNIA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CD4 ANTIGEN; HLA DQ ANTIGEN; HLA DR7 ANTIGEN;

AMINO ACID SEQUENCE; CELIAC DISEASE; CLINICAL FEATURE; DIARRHEA; EDITORIAL; GENETIC RISK; HLA SYSTEM; HUMAN; MALABSORPTION; PATHOGENESIS; PRIORITY JOURNAL; RISK FACTOR; SYMPTOM; T LYMPHOCYTE ACTIVATION; WASTING SYNDROME;

EID: 0036729951     PISSN: 00165085     EISSN: None     Source Type: Journal    
DOI: 10.1053/gast.2002.35840     Document Type: Article

References (43)

1. The coeliac iceberg in Italy. A multicentre antigliadin antibodies screening for coeliac disease in school-age subjects
2. Celiac disease risk in the USA: High prevalence of antiendomysium antibodies in healthy blood donors
3. High prevalence rates of adult silent coeliac disease, as seen in Sweden, must be expected in Denmark
4. Diagnosis of celiac sprue
5. Prevalence of hypertransaminasemia in adult celiac patients and effect of gluten-free diet
6. Celiac disease in patients with severe liver disease: Gluten-free diet may reverse hepatic failure
7. Celiac disease and irritable bowel-type symptoms
8. Occurrence of celiac disease after onset of type 1 diabetes: A 6-year prospective longitudinal study
9. Celiac disease during interferon treatment
10. Onset of coeliac disease during treatment with interferon for chronic hepatitis C
11. Interferon and ribavirin treatment for chronic hepatitis C may activate celiac disease
12. Evidence for a primary association of celiac disease to a particular HLA-DQ α/β heterodimer
13. HLA genes in coeliac disease
14. T lymphocyte recognition of a celiac disease-associated cis- or trans- encoded HLA-DQ α/β-heterodimer
15. The primary association of celiac disease to a given HLA-DQ α/β heterodimer explains the divergent HLA-DR associations observed in various Caucasian populations
16. T cells from the small intestinal mucosa of a DR4, DQ7/DR4, DQ8 celiac disease patient preferentially recognize gliadin when presented by DQ8
17. Function of DQ2 and DQ8 as HLA susceptibility molecules in celiac disease
18. Gliadin-specific, HLA-DQ(α 1*0501,β 1*0201) restricted T cells isolated from the small intestinal mucosa of celiac disease patients
19. Binding of peptides from the N-terminal region of α-gliadin to the celiac disease-associated HLA-DQ2 molecule assessed in biochemical and T cell assays
20. Identification of a gliadin T-cell epitope in coeliac disease: General importance of gliadin deamidation for intestinal T-cell recognition
21. Identification of the autoantigen of celiac disease
22. Both α and β chain polymorphisms determine the specificity of the disease-associated HLA-DQ2 molecules, with β chain residues being most influential
23. Peptide binding characteristics of the coeliac disease-associated DQ(α1*0501, β1*0201) molecule
24. Selective deamidation by tissue transglutaminase strongly enhances gliadin-specific T cell reactivity
25. Tissue transglutaminase selectively modifies gliadin peptides that are recognized by gut-derived T cells in celiac disease
26. In vivo antigen challenge in celiac disease identifies a single transglutaminase-modified peptide as the dominant A-gliadin T-cell epitope
27. The intestinal T cell response to α-gliadin in adult celiac disease is focused on a single deamidated glutamine targeted by tissue transglutaminase
28. The gluten response in children with celiac disease is directed toward multiple gliadin and glutenin peptides
29. Glutenin is involved in the gluten-driven mucosal T cell response
30. Specificity of tissue transglutaminase explains cereal toxicity in celiac disease
31. A comparison of diets with and without oats in adults with celiac disease
32. No harm from five year ingestion of oats in coeliac disease
33. Celiac lesion T cells recognize epitopes that cluster in regions of gliadins rich in proline residues
34. T cells from celiac disease lesions recognize gliadin epitopes deamidated in situ by endogenous tissue transglutaminase
35. Definition of the initial immunologic modifications upon in vitro gliadin challenge in the small intestine of celiac patients
36. Increased proinflammatory cytokine gene expression in the colonic mucosa of coeliac disease patients in the early period after gluten challenge
37. Intestinal digestive resistance of immunodominant gliadin peptides
38. Linkage analysis of candidate regions for coeliac disease genes
39. Genome search in celiac disease
40. A genome-wide family-based linkage study of coeliac disease
41. Genome-wide linkage analysis of Scandinavian affected sib-pairs supports presence of susceptibility loci for celiac disease on chromosomes 5 and 11
42. Genomewide linkage analysis of celiac disease in Finnish families
43. Existence of a genetic risk factor on chromosome 5q in Italian coeliac disease families