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本文采用新生小鼠锈导的移植耐受(NITT)模型。探讨了新生期过继转移成年同系鼠腹腔渗出细胞(PEC)对诱导移植耐受的影响。实验结果表明,新生小鼠(CFW、C57BL/6)单接受杂交一代小鼠(F_1)脾与淋巴结细胞后,诱导了特异性移植耐受(F_1组),耐受鼠百分率分别为57.7％与71.4％。如新生小鼠接受F_1 细胞前先接受 PEC 转移(PEC 组),则耐受的诱导受阻抑,耐受率为 0,MLR 的平均相对反应率(RR ％)增高,P<0.001;而与正常对照组比较,均无显著差异。 实验结果又表明,转移去T细胞的 PEC仍能阻抑CFW与 C57BL/6小鼠耐受的诱导,MLR的RR ％增高,P<0.001及<0.05;而转移非粘附性PEC组的RR ％与 F_1组无显著差异,耐受的诱导未受明显影响(P>0.3)。这提示 PEC中起阻抑耐受诱导作用的主要细胞是 Mφ,新生小鼠Mφ辅助功能缺陷可能是 NITT模型建立的重要原因。
In this paper, the newborn mouse rust-induced transplant tolerance (NITT) model. To explore the impact of neonatal adoptive transfer of adult rat cortical peritoneal exudate cells (PEC) on the induction of transplantation tolerance. The experimental results showed that the newborn mice (CFW, C57BL / 6) induced the specific transplantation tolerance (F_1 group) after single-hybrid generation (F_1) spleen and lymph node cells, the percent of tolerated mice were 57.7% 71.4%. For example, when newborn mice received PEC before receiving F_1 cells (PEC group), the induction of tolerance was inhibited, the tolerability rate was 0, and the mean relative response rate (RR%) of MLR increased (P <0.001) The control group, no significant difference. The results also showed that PEC transfected to T cells could still inhibit the tolerance of CFW and C57BL / 6 mice, the RR% of MLR increased, P <0.001 and <0.05, while the RR of non-adherent PEC % And F_1 group no significant difference in tolerance induction was not significantly affected (P> 0.3). This suggests that the primary cell that plays a role in repressing tolerance in PEC is Mφ, and Mφ helper dysfunction in neonatal mice may be an important reason for the establishment of NITT model.