<<Disclaimer: Verify this information before applying it to your situation.>> I just wanted to comment on the following articles which were just cited on PubMed. In these articles, it is found that there appears to be an absence of "double positive" CD4CD8 T cells in celiacs, on both GF and non-GF diets. Coincidentally I have been in the process of preparing a near- future posting about tin as an essential trace element on this List which, in part, briefly discusses the function of the thymus gland. It just so happens that the thymus gland is a central and primary site where large numbers of these "double positive" CD4CD8 T cells are generated. The thymus gland is particularly sensitive to malnutrition and to essential trace element deficiencies, especially zinc. Since celiac disease is a malabsorption disease, one would expect the thymus gland and its T cell production to be very much affected by celiac disease. I believe the article's finding of depleted "double positive" CD4CD8 T cells in celiacs is a result of malabsorption and mineral deficiences rather than some inherent part of the pathogenesis of celiac disease. However, these articles can be taken as evidence that the thymus gland is indeed affected by celiac disease. I'll have more about the thymus gland in my future posting on tin. ---------- Eur J Gastroenterol Hepatol. 2004 Oct;16(10):957-8. Intra-epithelial T cells in coeliac disease. Watson RG, Johnston SD. Dept of Medicine, Institute of Clinical Science, Royal Victoria Hospital, Belfast; and Dept of Gastroenterology, Belfast City Hospital, Belfast, UK. In coeliac disease dietary gliadin is damaging to the small intestinal mucosa.It occurs in individuals with a genetic predisposition.In terms of pathogenesis the link between genetics and the toxic effects of gliadin remains obscure. A study in this issue of the Journal demonstrates an inherent absence of double positive CD4CD8 T cells in coeliac patients. It is suggested that this could result in a loss of oral tolerance and play a role in the mucosal damage of coeliac disease. In addition, it is confirmed that intra-epithelial lymphocytes are not increased in coeliac disease but there is an apparent increase due to the change in architecture, and decrease in enterocytes. Coeliac disease is an enteropathy associated with dietary gluten which occurs in individuals with a genetic predisposition. The pathogenesis remains obscure although it is clear that only certain parts of the gliadin molecule are toxic and there is considerable evidence of immunological activity, including antibody production. In this issue of European Journal of Gastroenterology and Hepatology Carton et al. present evidence in favour of an inherent depletion of CD4CD8 T cells, which could result in a loss of oral tolerance to ingested gliadin. Using flow cytometry they also demonstrated that the classic T-cell infiltration of coeliac disease is not due to an increase in T cells but is an apparent increase associated with a relative decrease in enterocytes as a result of the change in architecture of the mucosa. These could be important fundamental observations in helping to unravel the pathogenesis of coeliac disease. PMID: 15371916 [PubMed - in process] ---------- Eur J Gastroenterol Hepatol. 2004 Oct;16(10):961-8. CD4+CD8+ human small intestinal T cells are decreased in coeliac patients, with CD8 expression downregulated on intra-epithelial T cells in the active disease. Carton J, Byrne B, Madrigal-Estebas L, O'Donoghue DP, O'Farrelly C. Education and Research Centre and Dept of Gastroenterology, St Vincent's University Hospital, Dublin; Institute of Immunology, National University of Ireland Maynooth, Co. Kildare; and Conway Institute, University College Dublin, Ireland. BACKGROUND/OBJECTIVE: The intestinal lesion of coeliac disease is thought to be initiated and exacerbated by dysregulation of local T-lymphocyte sub- populations. This study examines changes in intestinal T cells from coeliac patients, with a particular focus on CD4CD8 T cells, immunoregulatory cells normally found in relatively high proportions in the small intestine. METHODS: Cells were obtained from duodenal biopsies from active and treated coeliac patients using chelating and reducing agents (epithelial layer) followed by collagenase treatment (lamina propria). Cell yield and viability were assessed and flow cytometric analysis was used to examine CD4CD8 T cells and to quantify CD8 expression. RESULTS: Surprisingly, total T-cell yields in the epithelial layer did not increase in active coeliac disease although enterocyte counts decreased significantly, giving an appearance of infiltration. In active coeliac patients, CD4CD8 T cell percentages were significantly decreased in both the epithelial layer and lamina propria. Levels of CD8 expression by CD4CD8 T cells in the epithelial layer were decreased significantly in patients with active coeliac disease. CD4CD8 T cell proportions did not return to normal in treated coeliac patients whose villous architecture had responded to gluten withdrawal. CONCLUSIONS: No increase of intra-epithelial lymphocytes in the coeliac lesion may require us to reconsider the definition of coeliac disease as an inflammatory condition. Low CD4CD8 populations in treated as well as untreated coeliac patients indicate that these T cells are inherently absent in individuals genetically predisposed to coeliac disease. PMID: 15371918 [PubMed - in process] * * * * Please remember some posters may be WHEAT-FREE, but not GLUTEN-FREE *