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Concise Publication Free access | 10.1172/JCI106958

Predominance of histocompatibility antigen HL-A8 in patients with gluten-sensitive enteropathy

Z. Myron Falchuk, G. Nicholas Rogentine, and Warren Strober

Digestive and Hereditary Diseases Branch, National Institute of Arthritis and Metabolic Diseases, National Institutes of Health, Bethesda, Maryland 20014

Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014

Metabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014

Find articles by Falchuk, Z. in: PubMed | Google Scholar

Digestive and Hereditary Diseases Branch, National Institute of Arthritis and Metabolic Diseases, National Institutes of Health, Bethesda, Maryland 20014

Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014

Metabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014

Find articles by Rogentine, G. in: PubMed | Google Scholar

Digestive and Hereditary Diseases Branch, National Institute of Arthritis and Metabolic Diseases, National Institutes of Health, Bethesda, Maryland 20014

Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014

Metabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014

Find articles by Strober, W. in: PubMed | Google Scholar

Published June 1, 1972 - More info

Published in Volume 51, Issue 6 on June 1, 1972
J Clin Invest. 1972;51(6):1602–1605. https://doi.org/10.1172/JCI106958.
© 1972 The American Society for Clinical Investigation
Published June 1, 1972 - Version history
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Abstract

HL-A phenotypes were determined in 24 unrelated patients with gluten-sensitive enteropathy (GSE) using a lymphocyte microcytotoxicity test. 21 of the 24 patients had HL-A8 in the second segregant series, a frequency of 0.875. In contrast, the HL-A8 frequency in 200 normal individuals was 0.215 (difference significant at P < 0.002), and in 6 patients with villous atrophy due to tropical sprue or hypogammaglobulinemia the HL-A8 frequency was 0.17 (difference from normal not significant). The HL-A types in the families of three HL-A8 positive patients with GSE indicated that the HL-A8 antigen was inherited as an autosomal dominant. Frequencies of the other HL-A antigens in the GSE group did not differ significantly from that of the normal group. These findings are compatible with the hypothesis that GSE is due to the presence of an abnormal “immune response (Ir) gene,” leading to the production of pathogenic antigluten antibody or, alternatively, to the presence of a particular membrane configuration leading to the binding of gluten to epithelial cells with subsequent tissue damage.

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