The interaction of dietary fibres with disulphide bonds (S-S) and a potential strategy to reduce the toxicity of the gluten proteins in coeliac disease

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dc.authorid0000-0002-7050-4082
dc.contributor.authorAdams, Gary G.
dc.contributor.authorKök, M. Şamil
dc.contributor.authorImran, Shahwar
dc.contributor.authorHarding, Stephen E.
dc.contributor.authorİlyas, Mohammad
dc.contributor.authorTatham, Arthur S.
dc.date.accessioned2021-06-23T18:56:33Z
dc.date.available2021-06-23T18:56:33Z
dc.date.issued2012
dc.departmentBAİBÜ, Mühendislik Fakültesi, Gıda Mühendisliği Bölümüen_US
dc.description.abstractWith a prevalence of 1% in western populations, coeliac disease (CD) is one of the better understood human leukocyte antigen system (HLA) linked disorders (Green and Cellier 2007). Despite the fact that CD shares immunological features with inflammatory bowel disease, it is characterized by: (1) a defined trigger (prolamins from wheat, barley and rye and in some individuals, oats); (2) the presence of HLA class II genes, HLA-DQ2 or HLA-DQ8, and (3) the generation of circulating auto antibodies to the enzyme tissue transglutaminase (TG2). TG2 catalyses the formation of a covalent bond between protein free amino groups and the g-carboxamide groups of glutamine residues, which constitute some 30-40 mol%, of the prolamins, this increases their affinity to HLA-DQ2 or HLA-DQ8 proteins (Schuppan 2000). As a result, CD4 T-helper 1 T-cell activation occurs, which can result in intestinal mucosal inflammation, malabsorption, and numerous secondary complications. When conducting severity assessments of coeliac disease, duodenal histology showing intraepithelial lymphocytosis, crypt hyperplasia, and various degrees of villous atrophy, in conjunction with clinical observations, are considered to be the gold standard for diagnosis.en_US
dc.identifier.doi10.5661/bger-28-115
dc.identifier.endpage130en_US
dc.identifier.issn0264-8725
dc.identifier.pmid22616484en_US
dc.identifier.scopus2-s2.0-84860908178en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage115en_US
dc.identifier.urihttps://doi.org/10.5661/bger-28-115
dc.identifier.urihttps://hdl.handle.net/20.500.12491/5027
dc.identifier.urihttps://www.tandfonline.com/doi/pdf/10.5661/bger-28-115?needAccess=true
dc.identifier.volume28en_US
dc.identifier.wosWOS:000329096800007en_US
dc.identifier.wosqualityN/Aen_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.institutionauthorKök, M. Şamil
dc.language.isoenen_US
dc.relation.ispartofBiotechnology and Genetic Engineering Reviewsen_US
dc.relation.publicationcategoryDiğeren_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectCoeliac Diseaseen_US
dc.subjectGluten Proteins
dc.subjectDietary Fibres
dc.subjectDisulphide Bonds
dc.titleThe interaction of dietary fibres with disulphide bonds (S-S) and a potential strategy to reduce the toxicity of the gluten proteins in coeliac diseaseen_US
dc.typeReview Articleen_US

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