Abstract
Objective To study the roles of CD4+ CD25+ Foxp3+ regulatory T cells (Treg) in the immune tolerance induced by portal vein injection of donor splenocytes. Methods C57BL/6 mice were selected as donors and Balb/c mice as recipients. The recipients were divided into 7 groups at random. Recipients in blank control group received RPMI 1640 via portal vein injection, and those in the donor-splenocytes group and recipients-splenocytes group received splenocytes of C57BL/6 mice and Balb/c mice through portal vein injection, respectively. The recipients in blank transplant group received RPMI 1640 via portal vein injection,and 7 days later skin of C57BL/6 mice was transplanted.The recipients in experimental control group and experimental group received splenocytes of Balb/c mice and C57BL/6 mice through portal vein injection, and 7 days later skin of C57BL/6 mice was transplanted. The recipients in third-party transplant group received splenocytes of C57BL/6 mice through portal vein injection, and 7 days later skin of C3H mice was transplanted. The survival time and histological changes of donor skin were observed. Flow cytometry was applied to detect the proportions of CD4+ CD25+ Foxp3+ Treg in the blood, spleen and liver in each group. Results The survival time of donor skin allograft was significantly longer in experimental group (19. 8±4. 6 days) than in blank transplant group, experimental control group and third-party transplant group, but did not maintain long-term survival. Seven days after transplantation,histological changes showed that the rejection was milder in experimental group than in blank transplant group and experimental control group. The proportion of CD4+ CD25+ Foxp3+ Treg was significantly higher in donor-splenocytes group than in recipients-splenocytes group and blank control group. Conclusion Portal vein injection of donor-derived splenocytes can prolong the survival time of the skin allograft specifically, and reduce its rejection. In this process,the CD4+ CD25+ Foxp3+ Treg may play a role in the mechanism. Key words: T-lymphocytes, regulatory; Portal vein; Immune tolerance; Atigens, CD4; Atigens,CD25
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