Celiac.com 07/23/2020 - Celiac disease is a common inflammatory autoimmune condition that is influenced by both genetic factors and environmental triggers. Researchers still don't know very much about the early genesis of celiac disease. A team of researchers recently set out to describe the interplay between type 2 transglutaminase (TG2), gliadin peptide 31-43 and anti-TG2 antibodies in celiac disease.
The team included Stefania Martucciello, Silvia Sposito, Carla Esposito, Gaetana Paolella, and Ivana Caputo. They are variously affiliated with the Department of Chemistry and Biology; and the European Laboratory for the Investigation of Food-Induced Diseases (ELFID) at the University of Salerno in Fisciano (SA), Italy
The immune-triggering potential of some gluten sequences are increased by the deamidation of specific glutamine residues by type 2 transglutaminase (TG2), an enzyme whose expression is up-regulated in the intestine of celiacs.
The α-gliadin peptide 31-43 is a short gluten chain that resists intestinal proteases, and which seems to modulate TG2 function in the gut. Interestingly, TG2 can also influence the biological activity of this α-gliadin peptide 31-43.
A strong auto-immune response to TG2 is a classic sign of celiac disease. Auto-antibodies exert biological effects on multiple cells. These effects partly overlap with those caused by α-gliadin peptide 31-43.
In their recent review, the team poses a scenario in which TG2, anti-TG2 antibodies and peptide 31-43 come together to synergistically trigger and promote celiac disease. If their hypothesis is correct, further study could help researchers better understand celiac development and potentially point the way to new measures of prevention and/or treatment for celiac disease.
Stay tuned for more articles on the role of TG2, anti-TG2 antibodies and peptide 31-43 in the development of celiac disease.
Read more at Int J Mol Sci. 2020 May; 21(10): 3673