RESUMEN
OBJECTIVES: It has been reported that CXCR3 is related to inflammatory cell infiltration. The purpose of this study was to investigate iodine-125-labeled CXCL10, a ligand of CXCR3, as a tracer targeting CXCR3 to detect acute rejection in a mouse skin transplant model. MATERIALS AND METHODS: The isograft and allograft skin models were established with BALB/c and C57BL/6 mouse skin, respectively, as donors and BALB/c mice as recipients. We used reverse transcriptase-polymerase chain reaction and immunochemistry staining to test CXCR3 expression. ¹²5I-labeled CXCL10 was produced with the iodogenic method. Allograft/isograft mice were examined with whole body autoradiography and ex vivo biodistribution after tail vein injection of ¹²5I-labeled CXCL10 on day 8 posttransplant. RESULTS: CXCR3 expression was higher in allograft tissue than in isograft control. ¹²5I-labeled CXCL10 was prepared with high specificity and affinity. Biodistribution results showed higher ¹²5I-labeled CXCL10 uptake in allograft tissue. The target-to-nontarget ratio was 3.01 ± 0.25 at 24 hours, a result higher than that shown in the isograft group. Pharmacokinetic analyses of ¹²5I-labeled CXCL10 showed that distribution half-life was 0.34 hour and the elimination half-life was 9.83 hours. Dynamic whole body autoradiography images of ¹²5I-labeled CXCL10 showed excellent graft visualization in the allograft compared with the isograft group at all checking points, with visualization much more obvious at 12 and 24 hours. CONCLUSIONS: These data suggest that CXCR3 is a promising imaging target for immune cell infiltration in early-stage acute rejection and ¹²5I-labeled CXCL10 can successfully image acute rejection with good pharmacokinetics.