Tumor necrosis factor-α induced protein 8 like 2 (TIPE2) is one of the newly discovered negative regulators for body’s immune balance. The present study aimed to investigate the effect of TIPE2 gene-modified human amniotic mesenchymal stem cells (hAD-MSCs) on immune tolerance. In this study, the TIPE2 over-expressed and the non-transfected hAD-MSCs were severally co-cultured with injured cardiomyocytes. Cell cycle and apoptosis were detected by flow cytometry. Cell viability was measured by MTT, and expressions of immune-related factors were detected by qRT-PCR and western blot. When compared with the empty vector-transfected hAD-MSCs, the TIPE2-overexpression hAD-MSCs co-cultured with injured cardiomyocytes show accelerated cell viability and declined apoptosis. After TIPE2 over-expression, the mRNA and protein levels of p38, extracellular signal-regulated kinases (ERK) and interferon-γ (INF-γ) notably decreased, whereas those of transforming growth factor-β (TGF-β) and interleukin-10 (IL-10) increased in a converse trend. This study suggested that TIPE2 may enhance the cellular immune tolerance in co-culture systems of hAD-MSCs and injured cardiomyocyte, providing a theoretical basis for the allogeneic heart transplantation.

肿瘤坏死因子-α诱导蛋白8样2（TIPE2）是新发现的机体免疫平衡负调节剂之一。本研究旨在研究TIPE2基因修饰的人羊膜间充质干细胞（hAD-MSCs）对免疫耐受的影响。在这项研究中，过度表达TIPE2和未转染的hAD-MSC与受损的心肌细胞共培养。流式细胞仪检测细胞周期和凋亡。MTT法检测细胞活力，qRT-PCR和western blot检测免疫相关因子的表达。与空载体转染的hAD-MSC相比，与受损心肌细胞共培养的TIPE2过表达hAD-MSC显示出加速的细胞存活力并减少了凋亡。在TIPE2之后过表达时，p38，细胞外信号调节激酶（ERK）和干扰素-γ（INF-γ）的mRNA和蛋白水平显着降低，而转化生长因子-β（TGF-β）和白细胞介素10（ IL-10）以相反的趋势增加。这项研究表明TIPE2可以增强hAD-MSC与受损心肌细胞共培养系统的细胞免疫耐受性，为同种异体心脏移植提供理论依据。