Background

Allogeneic transplantation immune tolerance is currently a hot research issue and soluble CD83(sCD83) is a novel immunomodulator with great potential in inducing transplantation tolerance.

Objective

To investigate the mechanism of the immune tolerance effect of sCD83 on rat liver transplantation.

Method

A rat liver transplantation model was established to study the effects of sCD83 on the expression levels of IL-2, IL-10, and TGF-β in peripheral blood and the mRNA expressions of foxp3, TGF-β, and Indoleamine 2,3-dioxygenase (IDO) in liver. The expression changes of costimulatory molecules CD80, CD86, and MHC-II on the surface of DC cells and the expressions of IDO ⁺ DC cell, TGF-β ⁺ CD4 ⁺ T cell, and CD4 ⁺ CD25 ⁺ Foxp3 ⁺ T cell were analyzed and compared.

Results

sCD83 alleviated the rejection activity index (RAI) of rat liver transplantation in the early stage, increased the expressions of TGF-β, IL-10 in peripheral blood and the mRNAs of IDO, TGF-β and foxp3 in the transplanted liver, and down-regulated the expressions of MHC-II, CD86, and CD80 in DC cells, resulting in significant increased numbers of tolerogenic TGF-β ⁺ CD4 ⁺ T cells, Treg cells, and IDO ⁺ DC cells with low expression.

Conclusion

sCD83 inhibited acute rejection after liver transplantation in an allogeneic rat, and the mechanism was associated with the effect that sCD83 increased the expression of TGF-β, activated IDO immunosuppressive pathway, and increased tolerogenic DC cells and Treg cells.

中文翻译：

---

可溶性CD83通过上调大鼠肝移植中的TGF-β和IDO分泌来抑制急性排斥反应

背景

异基因移植的免疫耐受性是目前研究的热点，可溶性CD83（sCD83）是一种新型的免疫调节剂，具有诱导移植耐受性的巨大潜力。

目的

探讨sCD83对大鼠肝移植免疫耐受作用的机制。

方法

建立大鼠肝移植模型，以研究sCD83对外周血IL-2，IL-10和TGF-β表达水平以及foxp3，TGF-β和吲哚胺2,3-的mRNA表达的影响。肝脏中的双加氧酶（IDO）。分析DC细胞表面共刺激分子CD80，CD86和MHC-II的表达变化以及IDO ⁺ DC细胞，TGF-β ⁺ CD4 ⁺ T细胞，CD4 ⁺ CD25 ⁺ Foxp3 ⁺ T细胞的表达。比较。

结果

sCD83减轻了大鼠肝移植早期的排斥活性指数（RAI），增加了外周血TGF-β，IL-10的表达以及移植肝中IDO，TGF-β和foxp3的mRNA的表达。调节DC细胞中MHC-II，CD86和CD80的表达，导致低表达的致耐受性TGF-β ⁺ CD4 ⁺ T细胞，Treg细胞和IDO ⁺ DC细胞的数量显着增加。

结论

sCD83抑制了同种异体大鼠肝移植后的急性排斥反应，其机制与sCD83增加TGF-β的表达，激活IDO免疫抑制途径以及增加耐受性DC细胞和Treg细胞的作用有关。