Therapeutic Targeting of Classical and Lectin Pathways of Complement Protects from Ischemia-Reperfusion-Induced Renal Damage

摘要: Ischemia-reperfusion injury is the major cause of delayed graft function in transplanted kidneys, an early event significantly affecting long-term and survival. Several studies rodents suggest that alternative pathway complement system plays a pivotal role renal ischemia-reperfusion injury. However, limited information currently available from humans larger animals. Here we demonstrated 30 minutes ischemia resulted induction C4d/C1q, C4d/MLB, MBL/MASP-2 deposits swine model The infusion C1-inhibitor led to significant reduction peritubular capillary glomerular C4d C5b-9 deposition. Moreover, complement-inhibiting treatment reduced numbers infiltrating CD163 + , SWC3a CD4a CD8a cells. administration inhibition tubular damage epithelial cells apoptosis. Interestingly, report focal C4d-deposition colocalizes with C1q MBL at levels also patients function. In conclusion, activation pathogenic classical lectin pathways ischemia-reperfusion−induced damage. Therefore, these two might represent novel therapeutic approach prevention kidney transplant recipients.