Jefferson Adams is a freelance writer living in San Francisco. He has covered Health News for http://Examiner.com, and provided health and medical content for http://Sharecare.com. His work has appeared in Antioch Review, Blue Mesa Review, CALIBAN, Hayden's Ferry Review, Huffington Post, the Mississippi Review, and Slate, among others.
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.