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肿瘤免疫反应与慢性创面微环境的相似性:间充质基质/干细胞的影响。

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

机构信息

Institute for Cellular and Molecular Medicine, Department of Immunology, SAMRC Extramural Unit for Stem Cell Research and Therapy, Faculty of Health Sciences, University of Pretoria, Private Bag X323, Arcadia, 0007, South Africa.

Department of Oral Pathology and Oral Biology, School of Dentistry, Faculty of Health Sciences, University of Pretoria, PO Box 1266, Pretoria 0001, South Africa.

出版信息

J Immunol Res. 2021 Mar 29;2021:6649314. doi: 10.1155/2021/6649314. eCollection 2021.

Abstract

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.

摘要

肿瘤的特征是慢性炎症状态,被视为永不愈合的伤口。间充质基质/干细胞(MSCs)被认为是一种可能的治疗选择。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)中的作用存在相互矛盾的报告。一些研究表明 MSCs 促进肿瘤发生,而另一些研究则表明相反的结果。为了更好地评估 MSCs 在 TME 中的作用,了解 MSCs 在慢性伤口中的作用可能会有所帮助。在这里,我们讨论了 MSCs 在慢性伤口中的作用,并将其推断到 TME 中。慢性伤口停留在伤口愈合的炎症阶段,而在 TME 的情况下,炎症和增殖阶段都被利用。慢性伤口中的 MSCs 促进巨噬细胞表型从促炎(M1)向抗炎(M2)的转变,从而抑制 T、B 和自然杀伤细胞,进而促进伤口愈合。在 TME 的情况下,据报道 MSCs 通过抑制 T、B 和自然杀伤细胞以及树突状细胞、细胞毒性 T 细胞和 Th1 相关细胞因子来促进肿瘤发生,从而促进肿瘤生长。然而,一些研究表明 MSCs 抑制肿瘤发生,这取决于 MSCs 的来源和涉及的特定介质。因此,MSCs 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 MSCs 是一种有效的治疗选择,可以对抗肿瘤进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1064/8024060/96ec31f19835/JIR2021-6649314.001.jpg

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