2nna: Difference between revisions

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==Overview==
==Overview==
The risk of celiac disease is strongly associated with human leukocyte, antigen (HLA) DQ2 and to a lesser extent with HLA DQ8. Although the, pathogenesis of HLA-DQ2-mediated celiac disease is established, the, underlying basis for HLA-DQ8-mediated celiac disease remains unclear. We, showed that T helper 1 (Th1) responses in HLA-DQ8-associated celiac, pathology were indeed HLA DQ8 restricted and that multiple, mostly, deamidated peptides derived from protease-sensitive sites of gliadin were, recognized. This pattern of reactivity contrasted with the more absolute, deamidation dependence and relative protease resistance of the dominant, gliadin peptide in DQ2-mediated disease. We provided a structural basis, for the selection of HLA-DQ8-restricted, deamidated gliadin peptides. The, data established that the molecular mechanisms underlying HLA-DQ8-mediated, celiac disease differed markedly from the HLA-DQ2-mediated form of the, disease. Accordingly, nondietary therapeutic interventions in celiac, disease might need to be tailored to the genotype of the individual.
The risk of celiac disease is strongly associated with human leukocyte antigen (HLA) DQ2 and to a lesser extent with HLA DQ8. Although the pathogenesis of HLA-DQ2-mediated celiac disease is established, the underlying basis for HLA-DQ8-mediated celiac disease remains unclear. We showed that T helper 1 (Th1) responses in HLA-DQ8-associated celiac pathology were indeed HLA DQ8 restricted and that multiple, mostly deamidated peptides derived from protease-sensitive sites of gliadin were recognized. This pattern of reactivity contrasted with the more absolute deamidation dependence and relative protease resistance of the dominant gliadin peptide in DQ2-mediated disease. We provided a structural basis for the selection of HLA-DQ8-restricted, deamidated gliadin peptides. The data established that the molecular mechanisms underlying HLA-DQ8-mediated celiac disease differed markedly from the HLA-DQ2-mediated form of the disease. Accordingly, nondietary therapeutic interventions in celiac disease might need to be tailored to the genotype of the individual.
 
==Disease==
Known diseases associated with this structure: Celiac disease, susceptibility to OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=146880 146880]], Celiac disease, susceptibility to OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=604305 604305]], Creutzfeldt-Jakob disease, variant, resistance to OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=604305 604305]], Multiple sclerosis, susceptibility to OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=604305 604305]]


==About this Structure==
==About this Structure==
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[[Category: Homo sapiens]]
[[Category: Homo sapiens]]
[[Category: Protein complex]]
[[Category: Protein complex]]
[[Category: Anderson, R.P.]]
[[Category: Anderson, R P.]]
[[Category: Henderson, K.N.]]
[[Category: Henderson, K N.]]
[[Category: Rossjohn, J.]]
[[Category: Rossjohn, J.]]
[[Category: Tye-Din, J.A.]]
[[Category: Tye-Din, J A.]]
[[Category: deamidated gluten peptide]]
[[Category: deamidated gluten peptide]]
[[Category: immune system]]
[[Category: immune system]]
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[[Category: post translational modification]]
[[Category: post translational modification]]


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