A 10-residue peptide from durum wheat promotes a shift from a Th1-type response toward a Th2-type response in celiac disease  

Oleh:

Silano, Marco ; Benedetto, Rita Di ; Maialetti, Francesca ; Vincenzi, Alessandro De

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: The American Journal of Clinical Nutrition vol. 87 no. 02 (Feb. 2008), page 415.
Topik: Th1-to-Th2 shift ; gluten-specific T cells ; celiac disease

Ketersediaan

Perpustakaan FK Nomor Panggil: A07.K.2008.01 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Background: Celiac disease (CD) is a Th1-driven autoimmune permanent enteropathy that is triggered by dietary gluten. Molecules able to shift the immune response from a Th1- to a Th2-type response have been suggested as therapeutic agents for Th1 autoimmune diseases. Objective: We sought to investigate the possibility that a decapeptide from durum wheat (p10mer, QQPQDAVQPF), which was previously shown to prevent the activation of celiac peripheral lymphocytes, may promote a shift from a Th1- to a Th2-type immune response in gluten-specific intestinal T cells of CD patients. Design: Intestinal T lymphocyte lines derived from 8 children with CD were incubated with gliadin peptides both alone and simultaneously with p10mer. Cell proliferation and the production of interferon- and interleukin-10 by these T cells were measured. Results: The incubation of celiac intestinal T cells with deamidated gliadin peptides resulted in a significant (P < 0.008) increase in cell proliferation and interferon- release, whereas the simultaneous exposure to p10mer totally abolished the cell proliferation and cytokine release. Moreover, incubation with p10mer maintained an elevated release of interleukin-10, whereas exposure of the cells to culture medium only did not. The replacement of the residues of aspartic acid in position 5 or those of alanine in position 6 in the sequence of p10mer resulted in peptides with no activity in the activation experiments. Conclusion: In vitro, p10mer showed the ability to shift the pathogenic immune response of a CD patient from a Th1- to a Th2-type response.

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