Jefferson Adams is a freelance writer living in San Francisco. His poems, essays and photographs have appeared in Antioch Review, Blue Mesa Review, CALIBAN, Hayden's Ferry Review, Huffington Post, the Mississippi Review, and Slate among others.
He is a member of both the National Writers Union, the International Federation of Journalists, and covers San Francisco Health News for Examiner.com.
A patient with childhood celiac disease, who had undergone an allogeneic bone marrow transplant (BMT) for chronic myelogenous leukemia, was able to safely resume eating gluten after his celiac disease vanished.
Celiac.com 01/06/2014 - A team of researchers recently set out to clarify the role of the immune system and intestinal epithelium in the origins of celiac disease.
The research team included S. Ben-Horin, S. Polak-Charcon,I. Barshack, O. Picard, E. Fudim, M. Yavzori, C. Avivi, C. Mardoukh, A. Shimoni, Y Chowers, Y. and Maor, of the Department of Gastroenterology in Chaim Sheba Medical Center at Tel-Aviv University, Tel Hashomer in Tel-Aviv, Israel.
For five years, the team followed a patient with childhood celiac disease who had undergone an allogeneic bone marrow transplant (BMT) for chronic myelogenous leukemia, and subsequently resumed consuming a gluten-containing diet.
Using standard serology testing, along with CFSE-based proliferation assays of peripheral blood CD4+ cells and of intestinal LPL towards gliadin-TTG antigens, the team assessed immunological memory to gliadin epitopes in both the control patient and in 5 newly diagnosed celiac patients.
They used combined immuno-histochemistry and fluorescent in-situ hybridiazation (FISH) to determine the origin of the intestinal lymphocytes.
They found that the patient remained healthy for more than 5 years of follow-up after receiving BMT from a HLA-matched woman, and ceasing the gluten-free diet. The continued to show negative periodic antibodies tests and unremarkable serial duodenal biopsies.
In vitro tests showed lack of a memory response of the patient's peripheral blood and lamina propria CD4+ T-cells towards TTG, gliadin or TTG-treated gliadin, whereas memory responses were common in the newly diagnosed celiac patients.
Immuno-FISH of post-BMT duodenal mucosa showed that all the epithelial cells had the chromosomal phenotype of XY. In contrast, CD45+ lymphocytic lineage cells were all donor-derived XX cells, presumably originating in the transplanted bone marrow and re-populating the intestinal wall.
The resolution of celiac disease after allogeneic BMT does occur, and is associated with absent gliadin-specific memory response, and with a dichotomous lymphocyte-epithelial chimeric intestine. These findings suggest that the origins of celiac disease are deeply connected to the immune system, rather than the epithelial area.