Fig 1: Screening of various hCXCL10-Fc and hCXCL9-Fc mutants for CXCR3 agonism and DPP-4 resistance: (A) Screening set-up: Ca++ influx is induced when CHO-Ki cells overexpressing human CXCR3A are stimulated by CXCR3A agonists. Upon release, Ca++ binds to the aequorin, leading to the emission of light (469 nm). (B) (a and c) Ca++ influx in CHO-Ki cells overexpressing CXCR3A induced by various human CXCL10-Fc and CXCL9-Fc fusion proteins that have not been pretreated with a human DPP-4. (b and d) Ca++ influx in CHO-Ki cells overexpressing CXCR3A induced by human CXCL10-Fc, Q-CXCL10-Fc, CXCL9-Fc, Q-CXCL9-Fc that have been pretreated with human DPP-4. Statistical analysis was performed comparing the DPP-4-treated vs. nontreated CXCL10-Fc and human CXCL9-Fc controls (Q—Glutamine, E—Glutamic acid, K—Lysine, L—Leucine, P—Proline, N—Asparagine). Significance was determined using a Student t test while comparing each group to the nonmodified compound (either CXCL10-Fc or CXCL9-Fc) and is shown on the left side of each symbol. *P ≤ 0.05, **P ≤ 0.01, ***P ≤ 0.001 was considered significant.