Similarities between Tumour Immune Response and Chronic Wound Microenvironment: Influence of Mesenchymal Stromal/Stem Cells.

Similarities between Tumour Immune Response and Chronic Wound Microenvironment: Influence of Mesenchymal Stromal/Stem Cells.
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DOI:
10.1155/2021/6649314
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发表时间:
2021
影响因子:
4.1
通讯作者:
Pepper MS
Pepper MS
中科院分区:
医学3区
文献类型:
--
作者:
Peta KT;Ambele MA;Pepper MS

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肿瘤以慢性炎症状态为特征,被认为是永远不会愈合的伤口。间充质基质/干细胞(MSCs)被认为是一种可能的治疗方案。虽然MSCs可以调节免疫系统,迁移到炎症部位,并且具有天然的免疫特权,但关于这些细胞在肿瘤微环境(TME)中的作用一直存在相互矛盾的报道。一些研究表明,骨髓间充质干细胞促进肿瘤发生,而另一些研究则相反。为了更好地评价MSCs在TME中的作用,了解MSCs在慢性创面中的作用可能会有所帮助。在这里,我们讨论间充质干细胞在慢性创面中的作用,并将其推论到TME。慢性创面停留在创面愈合的炎症阶段,而在TME的情况下,炎性和增殖期都被利用。慢性创面中的MSCs促进巨噬细胞表型由促炎(M1)向抗炎(M2)转变,从而抑制T、B和自然杀伤细胞,从而促进创面愈合。在TME的情况下,据报道,MSCs除了抑制树突状细胞、细胞毒性T细胞和Th1相关细胞因子外,还通过抑制T、B和自然杀伤细胞来促进肿瘤的发生,从而促进肿瘤的生长。然而,一些研究表明,MSCs抑制肿瘤发生取决于MSCs的来源和涉及的特定介质。因此,骨髓间充质干细胞在TME中的作用似乎很复杂,可能会导致不同的结果。缺乏令人信服的证据表明间充质干细胞是对抗肿瘤进展的有效治疗选择。
Tumours are characterized by a state of chronic inflammation and are regarded as wounds that never heal. Mesenchymal stromal/stem cells (MSCs) are being considered as a possible treatment option. While MSCs can regulate the immune system, migrate to sites of inflammation, and are naturally immune-privileged, there have been contradictory reports on the role of these cells in the tumour microenvironment (TME). Some studies have suggested that MSCs promote tumourigenesis while others have suggested the contrary. To better evaluate the role of MSCs in the TME, it may be helpful to understand the role of MSCs in chronic wounds. Here, we discuss the role of MSCs in chronic wounds and extrapolate this to the TME. Chronic wounds are stuck in the inflammatory phase of wound healing, while in the case of the TME, both the inflammatory and proliferative phases are exploited. MSCs in chronic wounds promote a switch in macrophage phenotype from proinflammatory (M1) to anti-inflammatory (M2), thereby suppressing T, B, and natural killer cells, consequently promoting wound healing. In the case of the TME, MSCs are reported to promote tumorigenesis by suppressing T, B, and natural killer cells in addition to dendritic cells, cytotoxic T cells, and Th1-associated cytokines, thereby promoting tumour growth. Some studies have however suggested that MSCs inhibit tumourigenesis, depending on the source of the MSCs and the specific mediators involved. Therefore, the role of MSCs in the TME appears to be complex and may result in variable outcomes. Compelling evidence to suggest that MSCs are an effective treatment option against tumour progression is lacking.
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