Background

Insulitis is defined by the presence of immune cells infiltrating in the pancreatic islets that might progress into the complete β-cell loss. The immunomodulatory properties of bone marrow-derived mesenchymal stem cells (BM-MSCs) have attracted much attention. This study aimed to evaluate the possible immunomodulatory effects of rat BM-MSCs and MSCs-derived insulin-producing cells (IPCs) in a mouse model of pancreatic insulitis.

Methods

Insulitis was induced in BALB/c mice using five consecutive doses of streptozotocin. MSCs or IPCs were directly injected into the pancreas of mice and their effects on the expression of Th subsets-related genes were evaluated.

Results

Both BM-MSCs and IPCs significantly reduced the expression of pancreatic Th1-related IFN-γ (P < 0.001 and P < 0.05, respectively) and T-bet genes (both P < 0.001). Moreover, the expression of IL-10 gene was significantly increased in IPC-treated compared to BM-MSC- or PBS-treated mice (P < 0.001 both comparisons).

Conclusions

BM-MSCs and IPCs could successfully suppress pathologic Th1 immune responses in the mouse model of insulitis. However, the marked increase in IL-10 gene expression by IPCs compared to BM-MSCs suggests that their simultaneous use at the initial phase of autoimmune diabetes might be a better option to reduce inflammation but these results need to be verified by further experiments.

中文翻译：

---

在链脲佐菌素诱导的胰腺炎小鼠模型中，体外衍生的胰岛素产生细胞调节 Th1 免疫反应并诱导 IL-10

背景

胰岛炎的定义是存在免疫细胞浸润胰岛，可能进展为完全的 β 细胞丧失。骨髓间充质干细胞（BM-MSCs）的免疫调节特性引起了广泛关注。本研究旨在评估大鼠 BM-MSCs 和 MSCs 衍生的胰岛素产生细胞 (IPCs) 在小鼠胰腺炎模型中可能的免疫调节作用。

方法

使用五次连续剂量的链脲佐菌素在 BALB/c 小鼠中诱导了胰岛炎。将MSCs或IPCs直接注射到小鼠的胰腺中，并评估它们对Th亚群相关基因表达的影响。

结果

BM-MSCs 和 IPCs 均显着降低胰腺 Th1 相关IFN-γ（分别为P < 0.001 和P < 0.05）和T-bet基因（均P < 0.001）的表达。此外，与 BM-MSC 或 PBS 处理的小鼠相比，IPC 处理的小鼠中IL - 10基因的表达显着增加（两个比较P < 0.001）。

结论

BM-MSCs 和 IPCs 可以成功地抑制胰岛炎小鼠模型中的病理性 Th1 免疫反应。然而，与 BM-MSCs 相比，IPCs 的IL-10基因表达显着增加表明，在自身免疫性糖尿病的初始阶段同时使用它们可能是减少炎症的更好选择，但这些结果需要通过进一步的实验来验证。