Histocompatibility Antigens Associated With Adult Cœliac Disease

Stokes, P. L.; Holmes, G. K. T.; Asquith, P.; Mackintosh, Pauline; Cooke, W. T.

doi:10.1016/s0140-6736(72)91330-x

Cited by 275 publications

(75 citation statements)

References 16 publications

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“…3). This value is strikingly similar to that found in patients with GSE unassociated with DH in two separate studies (7,19). In contrast, the frequency of HL-A8 in patients with DH unassociated with morphologic and immunologic evidence of intestinal disease was only 28% (two out of seven patients).…”

Section: Methodssupporting

confidence: 87%

Dermatitis Herpetiformis IMMUNOLOGIC CONCOMITANTS OF SMALL INTESTINAL DISEASE AND RELATIONSHIP TO HISTOCOMPATIBILITY ANTIGEN HL-A8

Gebhard¹,

Falchuk²,

Katz³

et al. 1974

J. Clin. Invest.

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Section: Methodssupporting

confidence: 87%

Dermatitis Herpetiformis IMMUNOLOGIC CONCOMITANTS OF SMALL INTESTINAL DISEASE AND RELATIONSHIP TO HISTOCOMPATIBILITY ANTIGEN HL-A8

Gebhard¹,

Falchuk²,

Katz³

et al. 1974

J. Clin. Invest.

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“…24 patients (60%) with GSE were HLA-B8 positive and 16 (40%) were HLA-B8 negative. The frequency of HLA-B8 in this group of patients with GSE was somewhat lower than that previously reported by us and others (3)(4)(5) because non-B8 patients were selected for study to equalize the size of the experimental groups. Such selections were made without prior knowledge of the patient's reactivity in organ culture.…”

Section: Hla Typesmentioning

confidence: 53%

“…In view ofthe known association of GSE with certain histocompatibility antigens (HLA-B8, HLA-DW3), (3)(4)(5)(6), we determined in the present study whether the deleterious effect of gluten in vitro is restricted by the patient's histocompatibility type. Accordingly, we examined small intestinal tissue from patients with GSE who were positive or negative for HLA-B8 and determined the susceptibility of the tissue in vitro to the cytotoxic effect of gluten protein.…”

Section: Introductionmentioning

confidence: 99%

Gluten-sensitive Enteropathy

Falchuk¹,

Nelson²,

Katz³

et al. 1980

J. Clin. Invest.

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A B S T R A C T We previously developed an in vitro organ culture system in which gluten exerts a toxic effect on intestinal mucosa of patients with active gluten-sensitive enteropathy. Gluten generally inhibits the epithelial cell maturation of intestinal biopsy specimens that otherwise occurs if the tissue is cultured for 24-48 h in a gluten-free medium. However, small intestinal mucosa from 15-20% of patients with proven gluten-sensitive enteropathy fails to manifest the expected gluten-induced damage in vitro. In the present study, we explored the relation between in vitro gluteninduced intestinal damage and the presence of HLA-B8.We determined whether the patients' histocompatibility type (HLA-B8 positive or negative) influenced the ability of gluten protein to inhibit epithelial cell maturation of cultured intestinal biopsy specimens from patients with gluten-sensitive enteropathy.Intestinal biopsies from 21 of 24 patients with gluten-sensitive enteropathy and HLA-B8 showed gluteninduced dacmage in vitro. On the other hand, intestinal biopsies from only 4 of 16 patients with gluten-sensitive enteropathy I)ut without HLA-B8 showed gluteninduced daimage in vitro. The difference in the effect of gluten in vitro between these two groups was statistically significant (P < 0.01). The data show a dichotomy between gluten-induced tissue damage in vivo and in vitro in HLA-B8 negative patients, suggesting that Presented in part at

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“…2 It is, therefore, perhaps not surprising to find that the human MHC class II gene region holds the largest number, and some of the longest recognized, associations with autoimmune diseases of any similar-sized region across the genome (Table 1). Early associations based on serological typing were established for multiple sclerosis, 3,4 type I diabetes 5,6 and celiac disease 7,8 which were subsequently resolved to specific human leukocyte antigen (HLA)-DR/DQ haplotypes. 9,10 Moreover, recent genomewide association studies using common single nucleotide polymorphism (SNP) markers have served to underline the remarkable contribution of this region in susceptibility to autoimmune disease, 11 which dwarfs any other genetic effect.…”

Section: Introductionmentioning

confidence: 99%

Regulation of major histocompatibility complex class II gene expression, genetic variation and disease

et al. 2009

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Major histocompatibility complex (MHC) class II molecules are central to adaptive immune responses and maintenance of selftolerance. Since the early 1970s, the MHC class II region at chromosome 6p21 has been shown to be associated with a remarkable number of autoimmune, inflammatory and infectious diseases. Given that a full explanation for most MHC class II disease associations has not been reached through analysis of structural variation alone, in this review we examine the role of genetic variation in modulating gene expression. We describe the intricate architecture of the MHC class II regulatory system, indicating how its unique characteristics may relate to observed associations with disease. There is evidence that haplotypespecific variation involving proximal promoter sequences can alter the level of gene expression, potentially modifying the emergence and expression of key phenotypic traits. Although much emphasis has been placed on cis-regulatory elements, we also examine the role of more distant enhancer elements together with the evidence of dynamic inter-and intra-chromosomal interactions and epigenetic processes. The role of genetic variation in such mechanisms may hold profound implications for susceptibility to common disease.

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Histocompatibility Antigens Associated With Adult Cœliac Disease

Cited by 275 publications

References 16 publications

Dermatitis Herpetiformis IMMUNOLOGIC CONCOMITANTS OF SMALL INTESTINAL DISEASE AND RELATIONSHIP TO HISTOCOMPATIBILITY ANTIGEN HL-A8

Dermatitis Herpetiformis IMMUNOLOGIC CONCOMITANTS OF SMALL INTESTINAL DISEASE AND RELATIONSHIP TO HISTOCOMPATIBILITY ANTIGEN HL-A8

Gluten-sensitive Enteropathy

Regulation of major histocompatibility complex class II gene expression, genetic variation and disease

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