Celiac disease T-cell epitopes from gamma-gliadins: immunoreactivity depends on the genome of origin, transcript frequency, and flanking protein variation
<p<Abstract</p< <p<Background</p< <p<Celiac disease (CD) is caused by an uncontrolled immune response to gluten, a heterogeneous mixture of wheat storage proteins. The CD-toxicity of these proteins and their derived peptides is depending on the presence of specific T-ce...
Ausführliche Beschreibung
Autor*in: |
Salentijn Elma MJ [verfasserIn] Mitea D [verfasserIn] Goryunova Svetlana V [verfasserIn] van der Meer Ingrid M [verfasserIn] Padioleau Ismael [verfasserIn] Gilissen Luud JWJ [verfasserIn] Koning Frits [verfasserIn] Smulders Marinus JM [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2012 |
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Übergeordnetes Werk: |
In: BMC Genomics - BMC, 2003, 13(2012), 1, p 277 |
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Übergeordnetes Werk: |
volume:13 ; year:2012 ; number:1, p 277 |
Links: |
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DOI / URN: |
10.1186/1471-2164-13-277 |
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Katalog-ID: |
DOAJ065167635 |
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520 | |a <p<Abstract</p< <p<Background</p< <p<Celiac disease (CD) is caused by an uncontrolled immune response to gluten, a heterogeneous mixture of wheat storage proteins. The CD-toxicity of these proteins and their derived peptides is depending on the presence of specific T-cell epitopes (9-mer peptides; CD epitopes) that mediate the stimulation of HLA-DQ2/8 restricted T-cells. Next to the thoroughly characterized major T-cell epitopes derived from the α-gliadin fraction of gluten, γ-gliadin peptides are also known to stimulate T-cells of celiac disease patients. To pinpoint CD-toxic γ-gliadins in hexaploid bread wheat, we examined the variation of T-cell epitopes involved in CD in γ-gliadin transcripts of developing bread wheat grains.</p< <p<Results</p< <p<A detailed analysis of the genetic variation present in γ-gliadin transcripts of bread wheat (<it<T. aestivum</it<, allo-hexaploid, carrying the A, B and D genome), together with genomic γ-gliadin sequences from ancestrally related diploid wheat species, enabled the assignment of sequence variants to one of the three genomic γ-gliadin loci, <it<Gli-A1</it<, <it<Gli-B1</it< or <it<Gli-D1</it<. Almost half of the γ-gliadin transcripts of bread wheat (49%) was assigned to locus <it<Gli-D1</it<. Transcripts from each locus differed in CD epitope content and composition. The <it<Gli-D1</it< transcripts contained the highest frequency of canonical CD epitope cores (on average 10.1 per transcript) followed by the <it<Gli-A1</it< transcripts (8.6) and the <it<Gli-B1</it< transcripts (5.4). The natural variants of the major CD epitope from γ-gliadins, DQ2-γ-I, showed variation in their capacity to induce <it<in vitro</it< proliferation of a DQ2-γ-I specific and HLA-DQ2 restricted T-cell clone.</p< <p<Conclusions</p< <p<Evaluating the CD epitopes derived from γ-gliadins in their natural context of flanking protein variation, genome specificity and transcript frequency is a significant step towards accurate quantification of the CD toxicity of bread wheat. This approach can be used to predict relative levels of CD toxicity of individual wheat cultivars directly from their transcripts (cDNAs).</p< | ||
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10.1186/1471-2164-13-277 doi (DE-627)DOAJ065167635 (DE-599)DOAJ1c7ef484b2b74b9d87dcc960ac63e3cd DE-627 ger DE-627 rakwb eng TP248.13-248.65 QH426-470 Salentijn Elma MJ verfasserin aut Celiac disease T-cell epitopes from gamma-gliadins: immunoreactivity depends on the genome of origin, transcript frequency, and flanking protein variation 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<Celiac disease (CD) is caused by an uncontrolled immune response to gluten, a heterogeneous mixture of wheat storage proteins. The CD-toxicity of these proteins and their derived peptides is depending on the presence of specific T-cell epitopes (9-mer peptides; CD epitopes) that mediate the stimulation of HLA-DQ2/8 restricted T-cells. Next to the thoroughly characterized major T-cell epitopes derived from the α-gliadin fraction of gluten, γ-gliadin peptides are also known to stimulate T-cells of celiac disease patients. To pinpoint CD-toxic γ-gliadins in hexaploid bread wheat, we examined the variation of T-cell epitopes involved in CD in γ-gliadin transcripts of developing bread wheat grains.</p< <p<Results</p< <p<A detailed analysis of the genetic variation present in γ-gliadin transcripts of bread wheat (<it<T. aestivum</it<, allo-hexaploid, carrying the A, B and D genome), together with genomic γ-gliadin sequences from ancestrally related diploid wheat species, enabled the assignment of sequence variants to one of the three genomic γ-gliadin loci, <it<Gli-A1</it<, <it<Gli-B1</it< or <it<Gli-D1</it<. Almost half of the γ-gliadin transcripts of bread wheat (49%) was assigned to locus <it<Gli-D1</it<. Transcripts from each locus differed in CD epitope content and composition. The <it<Gli-D1</it< transcripts contained the highest frequency of canonical CD epitope cores (on average 10.1 per transcript) followed by the <it<Gli-A1</it< transcripts (8.6) and the <it<Gli-B1</it< transcripts (5.4). The natural variants of the major CD epitope from γ-gliadins, DQ2-γ-I, showed variation in their capacity to induce <it<in vitro</it< proliferation of a DQ2-γ-I specific and HLA-DQ2 restricted T-cell clone.</p< <p<Conclusions</p< <p<Evaluating the CD epitopes derived from γ-gliadins in their natural context of flanking protein variation, genome specificity and transcript frequency is a significant step towards accurate quantification of the CD toxicity of bread wheat. This approach can be used to predict relative levels of CD toxicity of individual wheat cultivars directly from their transcripts (cDNAs).</p< Wheat Gluten γ-gliadins Celiac disease T-cell epitopes Biotechnology Genetics Mitea D verfasserin aut Goryunova Svetlana V verfasserin aut van der Meer Ingrid M verfasserin aut Padioleau Ismael verfasserin aut Gilissen Luud JWJ verfasserin aut Koning Frits verfasserin aut Smulders Marinus JM verfasserin aut In BMC Genomics BMC, 2003 13(2012), 1, p 277 (DE-627)326644954 (DE-600)2041499-7 14712164 nnns volume:13 year:2012 number:1, p 277 https://doi.org/10.1186/1471-2164-13-277 kostenfrei https://doaj.org/article/1c7ef484b2b74b9d87dcc960ac63e3cd kostenfrei http://www.biomedcentral.com/1471-2164/13/277 kostenfrei https://doaj.org/toc/1471-2164 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2012 1, p 277 |
spelling |
10.1186/1471-2164-13-277 doi (DE-627)DOAJ065167635 (DE-599)DOAJ1c7ef484b2b74b9d87dcc960ac63e3cd DE-627 ger DE-627 rakwb eng TP248.13-248.65 QH426-470 Salentijn Elma MJ verfasserin aut Celiac disease T-cell epitopes from gamma-gliadins: immunoreactivity depends on the genome of origin, transcript frequency, and flanking protein variation 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<Celiac disease (CD) is caused by an uncontrolled immune response to gluten, a heterogeneous mixture of wheat storage proteins. The CD-toxicity of these proteins and their derived peptides is depending on the presence of specific T-cell epitopes (9-mer peptides; CD epitopes) that mediate the stimulation of HLA-DQ2/8 restricted T-cells. Next to the thoroughly characterized major T-cell epitopes derived from the α-gliadin fraction of gluten, γ-gliadin peptides are also known to stimulate T-cells of celiac disease patients. To pinpoint CD-toxic γ-gliadins in hexaploid bread wheat, we examined the variation of T-cell epitopes involved in CD in γ-gliadin transcripts of developing bread wheat grains.</p< <p<Results</p< <p<A detailed analysis of the genetic variation present in γ-gliadin transcripts of bread wheat (<it<T. aestivum</it<, allo-hexaploid, carrying the A, B and D genome), together with genomic γ-gliadin sequences from ancestrally related diploid wheat species, enabled the assignment of sequence variants to one of the three genomic γ-gliadin loci, <it<Gli-A1</it<, <it<Gli-B1</it< or <it<Gli-D1</it<. Almost half of the γ-gliadin transcripts of bread wheat (49%) was assigned to locus <it<Gli-D1</it<. Transcripts from each locus differed in CD epitope content and composition. The <it<Gli-D1</it< transcripts contained the highest frequency of canonical CD epitope cores (on average 10.1 per transcript) followed by the <it<Gli-A1</it< transcripts (8.6) and the <it<Gli-B1</it< transcripts (5.4). The natural variants of the major CD epitope from γ-gliadins, DQ2-γ-I, showed variation in their capacity to induce <it<in vitro</it< proliferation of a DQ2-γ-I specific and HLA-DQ2 restricted T-cell clone.</p< <p<Conclusions</p< <p<Evaluating the CD epitopes derived from γ-gliadins in their natural context of flanking protein variation, genome specificity and transcript frequency is a significant step towards accurate quantification of the CD toxicity of bread wheat. This approach can be used to predict relative levels of CD toxicity of individual wheat cultivars directly from their transcripts (cDNAs).</p< Wheat Gluten γ-gliadins Celiac disease T-cell epitopes Biotechnology Genetics Mitea D verfasserin aut Goryunova Svetlana V verfasserin aut van der Meer Ingrid M verfasserin aut Padioleau Ismael verfasserin aut Gilissen Luud JWJ verfasserin aut Koning Frits verfasserin aut Smulders Marinus JM verfasserin aut In BMC Genomics BMC, 2003 13(2012), 1, p 277 (DE-627)326644954 (DE-600)2041499-7 14712164 nnns volume:13 year:2012 number:1, p 277 https://doi.org/10.1186/1471-2164-13-277 kostenfrei https://doaj.org/article/1c7ef484b2b74b9d87dcc960ac63e3cd kostenfrei http://www.biomedcentral.com/1471-2164/13/277 kostenfrei https://doaj.org/toc/1471-2164 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2012 1, p 277 |
allfields_unstemmed |
10.1186/1471-2164-13-277 doi (DE-627)DOAJ065167635 (DE-599)DOAJ1c7ef484b2b74b9d87dcc960ac63e3cd DE-627 ger DE-627 rakwb eng TP248.13-248.65 QH426-470 Salentijn Elma MJ verfasserin aut Celiac disease T-cell epitopes from gamma-gliadins: immunoreactivity depends on the genome of origin, transcript frequency, and flanking protein variation 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<Celiac disease (CD) is caused by an uncontrolled immune response to gluten, a heterogeneous mixture of wheat storage proteins. The CD-toxicity of these proteins and their derived peptides is depending on the presence of specific T-cell epitopes (9-mer peptides; CD epitopes) that mediate the stimulation of HLA-DQ2/8 restricted T-cells. Next to the thoroughly characterized major T-cell epitopes derived from the α-gliadin fraction of gluten, γ-gliadin peptides are also known to stimulate T-cells of celiac disease patients. To pinpoint CD-toxic γ-gliadins in hexaploid bread wheat, we examined the variation of T-cell epitopes involved in CD in γ-gliadin transcripts of developing bread wheat grains.</p< <p<Results</p< <p<A detailed analysis of the genetic variation present in γ-gliadin transcripts of bread wheat (<it<T. aestivum</it<, allo-hexaploid, carrying the A, B and D genome), together with genomic γ-gliadin sequences from ancestrally related diploid wheat species, enabled the assignment of sequence variants to one of the three genomic γ-gliadin loci, <it<Gli-A1</it<, <it<Gli-B1</it< or <it<Gli-D1</it<. Almost half of the γ-gliadin transcripts of bread wheat (49%) was assigned to locus <it<Gli-D1</it<. Transcripts from each locus differed in CD epitope content and composition. The <it<Gli-D1</it< transcripts contained the highest frequency of canonical CD epitope cores (on average 10.1 per transcript) followed by the <it<Gli-A1</it< transcripts (8.6) and the <it<Gli-B1</it< transcripts (5.4). The natural variants of the major CD epitope from γ-gliadins, DQ2-γ-I, showed variation in their capacity to induce <it<in vitro</it< proliferation of a DQ2-γ-I specific and HLA-DQ2 restricted T-cell clone.</p< <p<Conclusions</p< <p<Evaluating the CD epitopes derived from γ-gliadins in their natural context of flanking protein variation, genome specificity and transcript frequency is a significant step towards accurate quantification of the CD toxicity of bread wheat. This approach can be used to predict relative levels of CD toxicity of individual wheat cultivars directly from their transcripts (cDNAs).</p< Wheat Gluten γ-gliadins Celiac disease T-cell epitopes Biotechnology Genetics Mitea D verfasserin aut Goryunova Svetlana V verfasserin aut van der Meer Ingrid M verfasserin aut Padioleau Ismael verfasserin aut Gilissen Luud JWJ verfasserin aut Koning Frits verfasserin aut Smulders Marinus JM verfasserin aut In BMC Genomics BMC, 2003 13(2012), 1, p 277 (DE-627)326644954 (DE-600)2041499-7 14712164 nnns volume:13 year:2012 number:1, p 277 https://doi.org/10.1186/1471-2164-13-277 kostenfrei https://doaj.org/article/1c7ef484b2b74b9d87dcc960ac63e3cd kostenfrei http://www.biomedcentral.com/1471-2164/13/277 kostenfrei https://doaj.org/toc/1471-2164 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2012 1, p 277 |
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10.1186/1471-2164-13-277 doi (DE-627)DOAJ065167635 (DE-599)DOAJ1c7ef484b2b74b9d87dcc960ac63e3cd DE-627 ger DE-627 rakwb eng TP248.13-248.65 QH426-470 Salentijn Elma MJ verfasserin aut Celiac disease T-cell epitopes from gamma-gliadins: immunoreactivity depends on the genome of origin, transcript frequency, and flanking protein variation 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<Celiac disease (CD) is caused by an uncontrolled immune response to gluten, a heterogeneous mixture of wheat storage proteins. The CD-toxicity of these proteins and their derived peptides is depending on the presence of specific T-cell epitopes (9-mer peptides; CD epitopes) that mediate the stimulation of HLA-DQ2/8 restricted T-cells. Next to the thoroughly characterized major T-cell epitopes derived from the α-gliadin fraction of gluten, γ-gliadin peptides are also known to stimulate T-cells of celiac disease patients. To pinpoint CD-toxic γ-gliadins in hexaploid bread wheat, we examined the variation of T-cell epitopes involved in CD in γ-gliadin transcripts of developing bread wheat grains.</p< <p<Results</p< <p<A detailed analysis of the genetic variation present in γ-gliadin transcripts of bread wheat (<it<T. aestivum</it<, allo-hexaploid, carrying the A, B and D genome), together with genomic γ-gliadin sequences from ancestrally related diploid wheat species, enabled the assignment of sequence variants to one of the three genomic γ-gliadin loci, <it<Gli-A1</it<, <it<Gli-B1</it< or <it<Gli-D1</it<. Almost half of the γ-gliadin transcripts of bread wheat (49%) was assigned to locus <it<Gli-D1</it<. Transcripts from each locus differed in CD epitope content and composition. The <it<Gli-D1</it< transcripts contained the highest frequency of canonical CD epitope cores (on average 10.1 per transcript) followed by the <it<Gli-A1</it< transcripts (8.6) and the <it<Gli-B1</it< transcripts (5.4). The natural variants of the major CD epitope from γ-gliadins, DQ2-γ-I, showed variation in their capacity to induce <it<in vitro</it< proliferation of a DQ2-γ-I specific and HLA-DQ2 restricted T-cell clone.</p< <p<Conclusions</p< <p<Evaluating the CD epitopes derived from γ-gliadins in their natural context of flanking protein variation, genome specificity and transcript frequency is a significant step towards accurate quantification of the CD toxicity of bread wheat. This approach can be used to predict relative levels of CD toxicity of individual wheat cultivars directly from their transcripts (cDNAs).</p< Wheat Gluten γ-gliadins Celiac disease T-cell epitopes Biotechnology Genetics Mitea D verfasserin aut Goryunova Svetlana V verfasserin aut van der Meer Ingrid M verfasserin aut Padioleau Ismael verfasserin aut Gilissen Luud JWJ verfasserin aut Koning Frits verfasserin aut Smulders Marinus JM verfasserin aut In BMC Genomics BMC, 2003 13(2012), 1, p 277 (DE-627)326644954 (DE-600)2041499-7 14712164 nnns volume:13 year:2012 number:1, p 277 https://doi.org/10.1186/1471-2164-13-277 kostenfrei https://doaj.org/article/1c7ef484b2b74b9d87dcc960ac63e3cd kostenfrei http://www.biomedcentral.com/1471-2164/13/277 kostenfrei https://doaj.org/toc/1471-2164 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2012 1, p 277 |
allfieldsSound |
10.1186/1471-2164-13-277 doi (DE-627)DOAJ065167635 (DE-599)DOAJ1c7ef484b2b74b9d87dcc960ac63e3cd DE-627 ger DE-627 rakwb eng TP248.13-248.65 QH426-470 Salentijn Elma MJ verfasserin aut Celiac disease T-cell epitopes from gamma-gliadins: immunoreactivity depends on the genome of origin, transcript frequency, and flanking protein variation 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<Celiac disease (CD) is caused by an uncontrolled immune response to gluten, a heterogeneous mixture of wheat storage proteins. The CD-toxicity of these proteins and their derived peptides is depending on the presence of specific T-cell epitopes (9-mer peptides; CD epitopes) that mediate the stimulation of HLA-DQ2/8 restricted T-cells. Next to the thoroughly characterized major T-cell epitopes derived from the α-gliadin fraction of gluten, γ-gliadin peptides are also known to stimulate T-cells of celiac disease patients. To pinpoint CD-toxic γ-gliadins in hexaploid bread wheat, we examined the variation of T-cell epitopes involved in CD in γ-gliadin transcripts of developing bread wheat grains.</p< <p<Results</p< <p<A detailed analysis of the genetic variation present in γ-gliadin transcripts of bread wheat (<it<T. aestivum</it<, allo-hexaploid, carrying the A, B and D genome), together with genomic γ-gliadin sequences from ancestrally related diploid wheat species, enabled the assignment of sequence variants to one of the three genomic γ-gliadin loci, <it<Gli-A1</it<, <it<Gli-B1</it< or <it<Gli-D1</it<. Almost half of the γ-gliadin transcripts of bread wheat (49%) was assigned to locus <it<Gli-D1</it<. Transcripts from each locus differed in CD epitope content and composition. The <it<Gli-D1</it< transcripts contained the highest frequency of canonical CD epitope cores (on average 10.1 per transcript) followed by the <it<Gli-A1</it< transcripts (8.6) and the <it<Gli-B1</it< transcripts (5.4). The natural variants of the major CD epitope from γ-gliadins, DQ2-γ-I, showed variation in their capacity to induce <it<in vitro</it< proliferation of a DQ2-γ-I specific and HLA-DQ2 restricted T-cell clone.</p< <p<Conclusions</p< <p<Evaluating the CD epitopes derived from γ-gliadins in their natural context of flanking protein variation, genome specificity and transcript frequency is a significant step towards accurate quantification of the CD toxicity of bread wheat. This approach can be used to predict relative levels of CD toxicity of individual wheat cultivars directly from their transcripts (cDNAs).</p< Wheat Gluten γ-gliadins Celiac disease T-cell epitopes Biotechnology Genetics Mitea D verfasserin aut Goryunova Svetlana V verfasserin aut van der Meer Ingrid M verfasserin aut Padioleau Ismael verfasserin aut Gilissen Luud JWJ verfasserin aut Koning Frits verfasserin aut Smulders Marinus JM verfasserin aut In BMC Genomics BMC, 2003 13(2012), 1, p 277 (DE-627)326644954 (DE-600)2041499-7 14712164 nnns volume:13 year:2012 number:1, p 277 https://doi.org/10.1186/1471-2164-13-277 kostenfrei https://doaj.org/article/1c7ef484b2b74b9d87dcc960ac63e3cd kostenfrei http://www.biomedcentral.com/1471-2164/13/277 kostenfrei https://doaj.org/toc/1471-2164 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2012 1, p 277 |
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In BMC Genomics 13(2012), 1, p 277 volume:13 year:2012 number:1, p 277 |
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Salentijn Elma MJ @@aut@@ Mitea D @@aut@@ Goryunova Svetlana V @@aut@@ van der Meer Ingrid M @@aut@@ Padioleau Ismael @@aut@@ Gilissen Luud JWJ @@aut@@ Koning Frits @@aut@@ Smulders Marinus JM @@aut@@ |
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Salentijn Elma MJ misc TP248.13-248.65 misc QH426-470 misc Wheat misc Gluten misc γ-gliadins misc Celiac disease misc T-cell epitopes misc Biotechnology misc Genetics Celiac disease T-cell epitopes from gamma-gliadins: immunoreactivity depends on the genome of origin, transcript frequency, and flanking protein variation |
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TP248.13-248.65 QH426-470 Celiac disease T-cell epitopes from gamma-gliadins: immunoreactivity depends on the genome of origin, transcript frequency, and flanking protein variation Wheat Gluten γ-gliadins Celiac disease T-cell epitopes |
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Celiac disease T-cell epitopes from gamma-gliadins: immunoreactivity depends on the genome of origin, transcript frequency, and flanking protein variation |
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celiac disease t-cell epitopes from gamma-gliadins: immunoreactivity depends on the genome of origin, transcript frequency, and flanking protein variation |
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Celiac disease T-cell epitopes from gamma-gliadins: immunoreactivity depends on the genome of origin, transcript frequency, and flanking protein variation |
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<p<Abstract</p< <p<Background</p< <p<Celiac disease (CD) is caused by an uncontrolled immune response to gluten, a heterogeneous mixture of wheat storage proteins. The CD-toxicity of these proteins and their derived peptides is depending on the presence of specific T-cell epitopes (9-mer peptides; CD epitopes) that mediate the stimulation of HLA-DQ2/8 restricted T-cells. Next to the thoroughly characterized major T-cell epitopes derived from the α-gliadin fraction of gluten, γ-gliadin peptides are also known to stimulate T-cells of celiac disease patients. To pinpoint CD-toxic γ-gliadins in hexaploid bread wheat, we examined the variation of T-cell epitopes involved in CD in γ-gliadin transcripts of developing bread wheat grains.</p< <p<Results</p< <p<A detailed analysis of the genetic variation present in γ-gliadin transcripts of bread wheat (<it<T. aestivum</it<, allo-hexaploid, carrying the A, B and D genome), together with genomic γ-gliadin sequences from ancestrally related diploid wheat species, enabled the assignment of sequence variants to one of the three genomic γ-gliadin loci, <it<Gli-A1</it<, <it<Gli-B1</it< or <it<Gli-D1</it<. Almost half of the γ-gliadin transcripts of bread wheat (49%) was assigned to locus <it<Gli-D1</it<. Transcripts from each locus differed in CD epitope content and composition. The <it<Gli-D1</it< transcripts contained the highest frequency of canonical CD epitope cores (on average 10.1 per transcript) followed by the <it<Gli-A1</it< transcripts (8.6) and the <it<Gli-B1</it< transcripts (5.4). The natural variants of the major CD epitope from γ-gliadins, DQ2-γ-I, showed variation in their capacity to induce <it<in vitro</it< proliferation of a DQ2-γ-I specific and HLA-DQ2 restricted T-cell clone.</p< <p<Conclusions</p< <p<Evaluating the CD epitopes derived from γ-gliadins in their natural context of flanking protein variation, genome specificity and transcript frequency is a significant step towards accurate quantification of the CD toxicity of bread wheat. This approach can be used to predict relative levels of CD toxicity of individual wheat cultivars directly from their transcripts (cDNAs).</p< |
abstractGer |
<p<Abstract</p< <p<Background</p< <p<Celiac disease (CD) is caused by an uncontrolled immune response to gluten, a heterogeneous mixture of wheat storage proteins. The CD-toxicity of these proteins and their derived peptides is depending on the presence of specific T-cell epitopes (9-mer peptides; CD epitopes) that mediate the stimulation of HLA-DQ2/8 restricted T-cells. Next to the thoroughly characterized major T-cell epitopes derived from the α-gliadin fraction of gluten, γ-gliadin peptides are also known to stimulate T-cells of celiac disease patients. To pinpoint CD-toxic γ-gliadins in hexaploid bread wheat, we examined the variation of T-cell epitopes involved in CD in γ-gliadin transcripts of developing bread wheat grains.</p< <p<Results</p< <p<A detailed analysis of the genetic variation present in γ-gliadin transcripts of bread wheat (<it<T. aestivum</it<, allo-hexaploid, carrying the A, B and D genome), together with genomic γ-gliadin sequences from ancestrally related diploid wheat species, enabled the assignment of sequence variants to one of the three genomic γ-gliadin loci, <it<Gli-A1</it<, <it<Gli-B1</it< or <it<Gli-D1</it<. Almost half of the γ-gliadin transcripts of bread wheat (49%) was assigned to locus <it<Gli-D1</it<. Transcripts from each locus differed in CD epitope content and composition. The <it<Gli-D1</it< transcripts contained the highest frequency of canonical CD epitope cores (on average 10.1 per transcript) followed by the <it<Gli-A1</it< transcripts (8.6) and the <it<Gli-B1</it< transcripts (5.4). The natural variants of the major CD epitope from γ-gliadins, DQ2-γ-I, showed variation in their capacity to induce <it<in vitro</it< proliferation of a DQ2-γ-I specific and HLA-DQ2 restricted T-cell clone.</p< <p<Conclusions</p< <p<Evaluating the CD epitopes derived from γ-gliadins in their natural context of flanking protein variation, genome specificity and transcript frequency is a significant step towards accurate quantification of the CD toxicity of bread wheat. This approach can be used to predict relative levels of CD toxicity of individual wheat cultivars directly from their transcripts (cDNAs).</p< |
abstract_unstemmed |
<p<Abstract</p< <p<Background</p< <p<Celiac disease (CD) is caused by an uncontrolled immune response to gluten, a heterogeneous mixture of wheat storage proteins. The CD-toxicity of these proteins and their derived peptides is depending on the presence of specific T-cell epitopes (9-mer peptides; CD epitopes) that mediate the stimulation of HLA-DQ2/8 restricted T-cells. Next to the thoroughly characterized major T-cell epitopes derived from the α-gliadin fraction of gluten, γ-gliadin peptides are also known to stimulate T-cells of celiac disease patients. To pinpoint CD-toxic γ-gliadins in hexaploid bread wheat, we examined the variation of T-cell epitopes involved in CD in γ-gliadin transcripts of developing bread wheat grains.</p< <p<Results</p< <p<A detailed analysis of the genetic variation present in γ-gliadin transcripts of bread wheat (<it<T. aestivum</it<, allo-hexaploid, carrying the A, B and D genome), together with genomic γ-gliadin sequences from ancestrally related diploid wheat species, enabled the assignment of sequence variants to one of the three genomic γ-gliadin loci, <it<Gli-A1</it<, <it<Gli-B1</it< or <it<Gli-D1</it<. Almost half of the γ-gliadin transcripts of bread wheat (49%) was assigned to locus <it<Gli-D1</it<. Transcripts from each locus differed in CD epitope content and composition. The <it<Gli-D1</it< transcripts contained the highest frequency of canonical CD epitope cores (on average 10.1 per transcript) followed by the <it<Gli-A1</it< transcripts (8.6) and the <it<Gli-B1</it< transcripts (5.4). The natural variants of the major CD epitope from γ-gliadins, DQ2-γ-I, showed variation in their capacity to induce <it<in vitro</it< proliferation of a DQ2-γ-I specific and HLA-DQ2 restricted T-cell clone.</p< <p<Conclusions</p< <p<Evaluating the CD epitopes derived from γ-gliadins in their natural context of flanking protein variation, genome specificity and transcript frequency is a significant step towards accurate quantification of the CD toxicity of bread wheat. This approach can be used to predict relative levels of CD toxicity of individual wheat cultivars directly from their transcripts (cDNAs).</p< |
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The CD-toxicity of these proteins and their derived peptides is depending on the presence of specific T-cell epitopes (9-mer peptides; CD epitopes) that mediate the stimulation of HLA-DQ2/8 restricted T-cells. Next to the thoroughly characterized major T-cell epitopes derived from the α-gliadin fraction of gluten, γ-gliadin peptides are also known to stimulate T-cells of celiac disease patients. To pinpoint CD-toxic γ-gliadins in hexaploid bread wheat, we examined the variation of T-cell epitopes involved in CD in γ-gliadin transcripts of developing bread wheat grains.</p< <p<Results</p< <p<A detailed analysis of the genetic variation present in γ-gliadin transcripts of bread wheat (<it<T. aestivum</it<, allo-hexaploid, carrying the A, B and D genome), together with genomic γ-gliadin sequences from ancestrally related diploid wheat species, enabled the assignment of sequence variants to one of the three genomic γ-gliadin loci, <it<Gli-A1</it<, <it<Gli-B1</it< or <it<Gli-D1</it<. Almost half of the γ-gliadin transcripts of bread wheat (49%) was assigned to locus <it<Gli-D1</it<. Transcripts from each locus differed in CD epitope content and composition. The <it<Gli-D1</it< transcripts contained the highest frequency of canonical CD epitope cores (on average 10.1 per transcript) followed by the <it<Gli-A1</it< transcripts (8.6) and the <it<Gli-B1</it< transcripts (5.4). The natural variants of the major CD epitope from γ-gliadins, DQ2-γ-I, showed variation in their capacity to induce <it<in vitro</it< proliferation of a DQ2-γ-I specific and HLA-DQ2 restricted T-cell clone.</p< <p<Conclusions</p< <p<Evaluating the CD epitopes derived from γ-gliadins in their natural context of flanking protein variation, genome specificity and transcript frequency is a significant step towards accurate quantification of the CD toxicity of bread wheat. 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