A 10-residue peptide from durum wheat promotes a shift from a Th1-type response toward a Th2-type response in celiac disease.
Am J Clin Nutr
; 87(2): 415-23, 2008 Feb.
Article
em En
| MEDLINE
| ID: mdl-18258633
ABSTRACT
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-gamma 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-gamma 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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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Triticum
/
Doença Celíaca
/
Citocinas
/
Células Th2
/
Células Th1
/
Gliadina
Limite:
Adolescent
/
Child
/
Child, preschool
/
Female
/
Humans
/
Male
Idioma:
En
Ano de publicação:
2008
Tipo de documento:
Article