Advertisement
Free access | 10.1172/JCI109848
Department of Medicine, Peter Bent Brigham Hospital, Boston, Massachusetts 02115
Department of Pediatrics (Gastroenterology Division), Peter Bent Brigham Hospital, Boston, Massachusetts 02115
Children's Hospital Medical Center, Harvard Medical School, Boston, Massachusetts 02115
Immunophysiology Branch, National Cancer Institute, Bethesda, Maryland 20205
Western Regional Research Center, U. S. Department of Agriculture, Berkeley, California 94710
Find articles by Falchuk, Z. in: JCI | PubMed | Google Scholar
Department of Medicine, Peter Bent Brigham Hospital, Boston, Massachusetts 02115
Department of Pediatrics (Gastroenterology Division), Peter Bent Brigham Hospital, Boston, Massachusetts 02115
Children's Hospital Medical Center, Harvard Medical School, Boston, Massachusetts 02115
Immunophysiology Branch, National Cancer Institute, Bethesda, Maryland 20205
Western Regional Research Center, U. S. Department of Agriculture, Berkeley, California 94710
Find articles by Nelson, D. in: JCI | PubMed | Google Scholar
Department of Medicine, Peter Bent Brigham Hospital, Boston, Massachusetts 02115
Department of Pediatrics (Gastroenterology Division), Peter Bent Brigham Hospital, Boston, Massachusetts 02115
Children's Hospital Medical Center, Harvard Medical School, Boston, Massachusetts 02115
Immunophysiology Branch, National Cancer Institute, Bethesda, Maryland 20205
Western Regional Research Center, U. S. Department of Agriculture, Berkeley, California 94710
Find articles by Katz, A. in: JCI | PubMed | Google Scholar
Department of Medicine, Peter Bent Brigham Hospital, Boston, Massachusetts 02115
Department of Pediatrics (Gastroenterology Division), Peter Bent Brigham Hospital, Boston, Massachusetts 02115
Children's Hospital Medical Center, Harvard Medical School, Boston, Massachusetts 02115
Immunophysiology Branch, National Cancer Institute, Bethesda, Maryland 20205
Western Regional Research Center, U. S. Department of Agriculture, Berkeley, California 94710
Find articles by Bernardin, J. in: JCI | PubMed | Google Scholar
Department of Medicine, Peter Bent Brigham Hospital, Boston, Massachusetts 02115
Department of Pediatrics (Gastroenterology Division), Peter Bent Brigham Hospital, Boston, Massachusetts 02115
Children's Hospital Medical Center, Harvard Medical School, Boston, Massachusetts 02115
Immunophysiology Branch, National Cancer Institute, Bethesda, Maryland 20205
Western Regional Research Center, U. S. Department of Agriculture, Berkeley, California 94710
Find articles by Kasarda, D. in: JCI | PubMed | Google Scholar
Department of Medicine, Peter Bent Brigham Hospital, Boston, Massachusetts 02115
Department of Pediatrics (Gastroenterology Division), Peter Bent Brigham Hospital, Boston, Massachusetts 02115
Children's Hospital Medical Center, Harvard Medical School, Boston, Massachusetts 02115
Immunophysiology Branch, National Cancer Institute, Bethesda, Maryland 20205
Western Regional Research Center, U. S. Department of Agriculture, Berkeley, California 94710
Find articles by Hague, N. in: JCI | PubMed | Google Scholar
Department of Medicine, Peter Bent Brigham Hospital, Boston, Massachusetts 02115
Department of Pediatrics (Gastroenterology Division), Peter Bent Brigham Hospital, Boston, Massachusetts 02115
Children's Hospital Medical Center, Harvard Medical School, Boston, Massachusetts 02115
Immunophysiology Branch, National Cancer Institute, Bethesda, Maryland 20205
Western Regional Research Center, U. S. Department of Agriculture, Berkeley, California 94710
Find articles by Strober, W. in: JCI | PubMed | Google Scholar
Published August 1, 1980 - More info
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 gluten-induced 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 gluten-induced damage in vitro. On the other hand, intestinal biopsies from only 4 of 16 patients with gluten-sensitive enteropathy but without HLA-B8 showed gluten-induced damage 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 HLA-B8 is important for gluten to manifest a cytotoxic influence in organ culture.