DPP4 can cleave 2 amino acids off the end of a number of chemokines, rendering the chemokine inactive. Collaborators at the Pasteur institute were interested in what effect inhibiting DPP4 would have on the level of the active chemokine forms. Using a new assay developed by our collaborators, the level of full-length (active form) and cleaved (inactive) CXCL10 were measured in healthy individuals before and after administration of either sitagliptin or placebo. During active DPP4 inhibition while taking sitagliptin, individuals showed a decrease in full length CXCL10 and an increase in the shorter inactive form. Therefore, DPP4 has a dominant role for processing CXCL10 in vivo.
| Decalf, Jérémie; Tarbell, Kristin V; Casrouge, Armanda et al. (2016) Inhibition of DPP4 activity in humans establishes its in vivo role in CXCL10 post-translational modification: prospective placebo-controlled clinical studies. EMBO Mol Med 8:679-83 |
| Price, J D; Linder, G; Li, W P et al. (2013) Effects of short-term sitagliptin treatment on immune parameters in healthy individuals, a randomized placebo-controlled study. Clin Exp Immunol 174:120-8 |
