Heather Julia Ellis
Affiliation: King's College London
- Antibodies to wheat high-molecular-weight glutenin subunits in patients with celiac diseaseH Julia Ellis
Division of Diabetes and Nutritional Sciences, King s College London, London, UK
Int Arch Allergy Immunol 159:428-34. 2012..The high-molecular-weight (HMW) glutenin subunits (GS)-1Dy10 are toxic for patients with celiac disease (CD). This study aimed to assess whether CD patients mount a serological response to HMW-GS-1Dy10...
- Should coeliac sufferers be allowed their oats?Heather Julia Ellis
Division of Nutritional Sciences, King s College London, London, England, UK
Eur J Gastroenterol Hepatol 20:492-3. 2008..Oats could form a potentially useful part of a gluten-free diet, but patients require careful advice and monitoring, backed by robust gluten-assay techniques...
- Investigation of the putative immunodominant T cell epitopes in coeliac diseaseH J Ellis
Gastroenterology Unit, Rayne Institute KCL, St Thomas Hospital, London, UK
Gut 52:212-7. 2003..Deamidation by tissue transglutaminase (tTG) of the glutamine (Q) at position 65 to glutamic acid (E) is essential for T cell stimulation...
- In vivo gluten challenge in celiac diseaseH J Ellis
Gastroenterology Unit, The Rayne Institute, St Thomas Hospital, London, United Kingdom
Can J Gastroenterol 15:243-7. 2001..This could result in an abnormal presentation to the immune system, triggering a pathogenic rather than a tolerogenic response...
- Characterizing one of the DQ2 candidate epitopes in coeliac disease: A-gliadin 51-70 toxicity assessed using an organ culture systemSusi Martucci
Gastroenterology Department, Rayne Institute KCL, St Thomas Hospital, London, UK
Eur J Gastroenterol Hepatol 15:1293-8. 2003..To investigate, using an organ culture system, in-vitro toxicity of region 51-70 of A-gliadin (SQQPYLQLQPFPQPQLPYSQ), a peptide overlapping some of the sequences recently characterized as DQ2-restricted T-cell epitopes in coeliac disease...
- CTLA-4/CD28 gene region is associated with genetic susceptibility to coeliac disease in UK familiesA L King
J Med Genet 39:51-4. 2002
- Analysis of candidate genes on chromosome 19 in coeliac disease: an association study of the KIR and LILR gene clustersS J Moodie
Gastroenteroly Unit, GKT, The Rayne Institute, St Trhomas Hospital, London, UK
Eur J Immunogenet 29:287-91. 2002..A transmission disequilibrium test also found no association of the A and B KIR haplotypes or the LILRA3 gene deletion with coeliac disease...
- Coeliac disease: follow-up linkage study provides further support for existence of a susceptibility locus on chromosome 11p11A L King
Gastroenterology Unit, GKT, The Rayne Institute, St. Thomas' Hospital, London, UK
Ann Hum Genet 65:377-86. 2001..6 at D11S914 on chromosome 11p11. This marker maps to a position implicated in one of the two previous genome scans and taken together these results provide strong support for the existence of a susceptibility locus in this region...
- Coeliac disease: in vivo toxicity of the putative immunodominant epitopeJ S Fraser
Gastroenterology Department, Rayne Institute KCL, St Thomas Hospital, London SE1 7EH, UK
Gut 52:1698-702. 2003..We wished to investigate whether a peptide corresponding to residues 56-75 of alpha-gliadins exacerbates coeliac disease in vivo...
- Human lymphocyte stimulation with pouchitis flora is greater than with flora from a healthy pouch but is suppressed by metronidazoleA J G Bell
Department of Gastroenterology, The Rayne Institute, 4th Floor Lambeth Wing, St Thomas Hospital, Lambeth Palace Road, London SE1 7EH, UK
Gut 53:1801-5. 2004..Using bacteria from patients the authors sought evidence for the presence rather than the identity of a pathogenic species in pouchitis, and for its absence in healthy pouches by the differential effect on lymphocyte proliferation...
- Human genome search in celiac disease using gliadin cDNA as probeR Kumar
Department of Cell Biology, University of Virginia, Charlottesville, VA 22908, USA
J Mol Biol 300:1155-67. 2000..Glutamine to glutamic acid or other mutation within such epitopes followed by injury or infection-related release could explain enhanced disease susceptibility in affected families...