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Recent reports suggest that complement system contributes to allograft rejection. However, its underlying mechanism is poorly understood. Herein, we investigate the role of complement component 3 (C3) in a single MHC-II molecule mismatched murine model of allograft rejection using C3 deficient mice (C3 −/− ) as skin graft donors or recipients. Compared with C3 +/+  B6 allografts, C3 −/−  B6 grafts dramatically prolonged survival in MHC-II molecule mismatched H-2 bm12  B6 recipients, indicating that C3 plays a critical role in allograft rejection. Compared with C3 +/+  allografts, both Th17 cell infiltration and Th1/Th17 associated cytokine mRNA levels were clearly reduced in C3 −/−  allografts. Moreover, C3 −/−  allografts caused attenuated Th1/Th17 responses, but increased CD4 + CD25 + Foxp3 +  regulatory T (Treg) cell expression markedly in local intragraft and H-2 bm12  recipients. Depletion of Treg cells by anti-CD25 monoclonal antibody (mAb) negated the survival advantages conferred by C3 deficiency. Our results indicate for the first time that C3 deficiency can prolong MHC-II molecule mismatched skin allograft survival, which is further confirmed to be associated with increased CD4 +  CD25 +  Treg cell population expansion and attenuated Th1/Th17 response.

Complement component 3 deficiency prolongs MHC-II disparate skin allograft survival by increasing the CD4+ CD25+ regulatory T cells population