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Peptic–tryptic Digest of Gliadin Differentiates Human Monocytes into Dendritic Cells Independently of the Presence of Celiac Disease and Genetic Make-up
- By Jefferson Adams
- Published 01/7/2010
- Celiac Disease & Gluten Intolerance Research
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Jefferson Adams
Jefferson Adams is a freelance writer living in San Francisco. His poems, essays and photographs have appeared in Antioch Review, Blue Mesa Review, CALIBAN, Hayden's Ferry Review, Huffington Post, the Mississippi Review, and Slate among others.
View all articles by Jefferson Adams
A team of researchers with the Department of Medicine at the University Erlangen-Nuernberg in Germany recently set out to examine the role of the innate immune system in celiac disease. The team included Maryam Rakhimova, Birgit Esslinger, Anja Schulze-Krebs, Eckhart G. Hahn, Detlef Schuppan and Walburga Dieterich.
The researchers matured dendritic cells taken from venous blood of patients with both active and with treated celiac disease, along with DQ2–DQ8-positive or negative control subjects. They treated the dendritic cells with a peptic–tryptic digest of gliadin (500 μg/ml)
and assessed activation by means of fluorescent-activated cell sorting analysis, cytokine secretion, and the cells' ability to trigger T cell proliferation.
The team noted that gliadin up-regulated interleukin (IL)-6, IL-8, and IL-12 (p40) secretion in dendritic cells and triggered clear expression of the maturation markers human leukocyte antigen (HLA)-DR, CD25, CD83, and CD86 in all test subjects, without regard to their genotype or the presence of disease; whereas the digest of bovine serum albumin had no effect.
However, gliadin-stimulated dendritic cells from patients with active celiac disease showed greater stimulation of autologous T cells compared to the other groups. The team concluded that further research should be aimed at identifying the mechanisms that control inflammation in healthy individuals.
Source:
J Clin Immunol, Volume 29, Number 1, January, 2009
The researchers matured dendritic cells taken from venous blood of patients with both active and with treated celiac disease, along with DQ2–DQ8-positive or negative control subjects. They treated the dendritic cells with a peptic–tryptic digest of gliadin (500 μg/ml)
and assessed activation by means of fluorescent-activated cell sorting analysis, cytokine secretion, and the cells' ability to trigger T cell proliferation.
The team noted that gliadin up-regulated interleukin (IL)-6, IL-8, and IL-12 (p40) secretion in dendritic cells and triggered clear expression of the maturation markers human leukocyte antigen (HLA)-DR, CD25, CD83, and CD86 in all test subjects, without regard to their genotype or the presence of disease; whereas the digest of bovine serum albumin had no effect.
However, gliadin-stimulated dendritic cells from patients with active celiac disease showed greater stimulation of autologous T cells compared to the other groups. The team concluded that further research should be aimed at identifying the mechanisms that control inflammation in healthy individuals.
Source:
J Clin Immunol, Volume 29, Number 1, January, 2009
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