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首页> 外文期刊>Cell and Tissue Research >CD4(+)CD25 (+) regulatory T cells are not required for mesenchymal stem cell function in fully MHC-mismatched mouse cardiac transplantation.
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CD4(+)CD25 (+) regulatory T cells are not required for mesenchymal stem cell function in fully MHC-mismatched mouse cardiac transplantation.

机译：在完全MHC不匹配的小鼠心脏移植中，间充质干细胞功能不需要CD4（+）CD25（+）调节性T细胞。

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摘要

Although the immunomodulative properties of mesenchymal stem cells (MSCs) open up attractive possibilities in solid-organ transplantation, information concerning the optimal dose, route, timing of administration, major histocompatibility complex (MHC)-restriction and relevant mechanisms is currently lacking. Therefore, better characterization of MSC immunoregulatory activity and elucidation of its mechanisms are crucial. In this study, we confirmed that MSCs did not elicit proliferation by allogeneic CD4(+) T cells, suggesting that MSCs were not immunogenic. By using C57BL/6 mouse MSCs as donor-derived or recipient-derived or as third-party MSCs, we discovered that MSCs suppressed CD4(+) T cell proliferation and prolonged mouse cardiac allograft survival in a dose-dependent and non-MHC-restricted manner. We also found that intraperitoneal administration favored survival prolongation, although this prolongation was weaker than that via the intravenous route. Only infusion at earlier time points favored survival prolongation. Depletion of CD4(+)CD25(+) T cells did not affect the immunosuppression of MSCs on CD4(+) T cells. Moreover, MSCs did not induce regulatory T cells. The in vivo data revealed that MSCs did not increase the percentage of CD4(+)CD25(+) T cells and FoxP3 expression. More importantly, we demonstrated for the first time that depletion of CD4(+)CD25(+) T cells did not hinder MSC-induced survival prolongation, indicating that CD4(+)CD25(+) regulatory T cells were not essential for the prolongation of MSC-mediated allograft survival.
机译：尽管间充质干细胞（MSCs）的免疫调节特性为固体器官移植开辟了诱人的可能性，但目前尚缺乏有关最佳剂量，途径，给药时间，主要组织相容性复合物（MHC）限制和相关机制的信息。因此，更好地表征MSC免疫调节活性及其机制至关重要。在这项研究中，我们证实了MSCs不会引起同种CD4（+）T细胞的增殖，这表明MSCs不是免疫原性的。通过使用C57BL / 6小鼠MSC作为供体来源或受体来源或第三方MSC，我们发现MSC抑制CD4（+）T细胞增殖，并在剂量依赖性和非MHC-受限制的方式。我们还发现腹膜内给药有利于延长生存期，尽管这种延长期比经静脉途径要弱。仅在较早的时间点输注有利于延长生存时间。 CD4（+）CD25（+）T细胞的耗竭并不影响MSC对CD4（+）T细胞的免疫抑制。而且，MSC不诱导调节性T细胞。体内数据显示，MSC不会增加CD4（+）CD25（+）T细胞和FoxP3表达的百分比。更重要的是，我们首次证明了CD4（+）CD25（+）T细胞的耗竭不会阻止MSC诱导的生存期延长，这表明CD4（+）CD25（+）调节性T细胞对于延长并非必需介导的同种异体移植存活率的变化。

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