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半乳糖凝集素-9 对于子宫内膜再生细胞诱导小鼠长期心脏移植物存活是必需的。

Galectin-9 is required for endometrial regenerative cells to induce long-term cardiac allograft survival in mice.

机构信息

Department of General Surgery, Tianjin Medical University General Hospital, 154 Anshan Road, Heping District, Tianjin, 300052, China.

Tianjin General Surgery Institute, Tianjin Medical University General Hospital, Tianjin, China.

出版信息

Stem Cell Res Ther. 2020 Nov 5;11(1):471. doi: 10.1186/s13287-020-01985-0.

DOI:10.1186/s13287-020-01985-0
PMID:33153471
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7643467/
Abstract

BACKGROUND

Endometrial regenerative cells (ERCs), a novel type of mesenchymal-like stem cells, were identified as an attractive candidate for immunoregulation and induction of cardiac allograft tolerance. However, the underlying mechanisms of ERCs in immune regulation still remain largely unclear. The present study is designed to determine whether the expression of Galectin-9 (Gal-9), a soluble tandem-repeat member of the galectin family, is crucial for ERC-based immunomodulation.

METHODS

In this study, we measured Gal-9 expression on ERCs and then co-cultured Gal-9-ERCs, ERCs, and ERCs+lactose (Gal-9 blocker) with activated C57BL/6-derived splenocytes. Furthermore, we performed mouse heart transplantation between BALB/c (H-2) donor and C57BL/6 (H-2) recipient. ERCs were administrated 24 h after the surgery, either alone or in combination with rapamycin.

RESULTS

Our data demonstrate that ERCs express Gal-9, and this expression is increased by IFN-γ stimulation in a dose-dependent manner. Moreover, both in vitro and in vivo results show that Gal-9-ERC-mediated therapy significantly suppressed Th1 and Th17 cell response, inhibited CD8 T cell proliferation, abrogated B cell activation, decreased donor-specific antibody production, and enhanced the Treg population. The therapeutic effect of ERCs was further verified by their roles in prolonging cardiac allograft survival and alleviating graft pathological changes.

CONCLUSIONS

Taken together, these data indicate that Gal-9 is required for ERC-mediated immunomodulation and prevention of allograft rejection.

摘要

背景

子宫内膜再生细胞（Endometrial regenerative cells，ERCs）是一种新型的间充质样干细胞，被认为是免疫调节和诱导心脏同种异体移植耐受的有吸引力的候选者。然而，ERC 在免疫调节中的潜在机制在很大程度上仍不清楚。本研究旨在确定半乳糖凝集素-9（Galectin-9，Gal-9）的表达是否对基于 ERC 的免疫调节至关重要，Gal-9 是半乳糖凝集素家族的可溶性串联重复成员。

方法

在这项研究中，我们测量了 ERCs 上 Gal-9 的表达，然后将 Gal-9-ERCs、ERC 和 ERCs+乳糖（Gal-9 阻断剂）与激活的 C57BL/6 来源的脾细胞共培养。此外，我们在 BALB/c（H-2）供体和 C57BL/6（H-2）受体之间进行了小鼠心脏移植。在手术后 24 小时，单独或与雷帕霉素联合给予 ERCs。

结果

我们的数据表明，ERC 表达 Gal-9，并且这种表达可被 IFN-γ 刺激以剂量依赖性方式增加。此外，体内外结果均表明，Gal-9-ERC 介导的治疗显著抑制 Th1 和 Th17 细胞反应，抑制 CD8 T 细胞增殖，破坏 B 细胞激活，减少供体特异性抗体产生，并增加 Treg 群体。ERC 延长心脏同种异体移植物存活和减轻移植物病理变化的作用进一步验证了其治疗效果。

结论

综上所述，这些数据表明 Gal-9 是 ERC 介导的免疫调节和预防同种异体排斥反应所必需的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47f7/7643467/f776ae9e4413/13287_2020_1985_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47f7/7643467/1f16f59d45be/13287_2020_1985_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47f7/7643467/375e9a9f2994/13287_2020_1985_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47f7/7643467/63c85c91d1b2/13287_2020_1985_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47f7/7643467/cecb4212e8a9/13287_2020_1985_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47f7/7643467/a0d134d209b4/13287_2020_1985_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47f7/7643467/ca77e76bdbcb/13287_2020_1985_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47f7/7643467/d75270dcd9b2/13287_2020_1985_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47f7/7643467/f776ae9e4413/13287_2020_1985_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47f7/7643467/1f16f59d45be/13287_2020_1985_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47f7/7643467/375e9a9f2994/13287_2020_1985_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47f7/7643467/63c85c91d1b2/13287_2020_1985_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47f7/7643467/cecb4212e8a9/13287_2020_1985_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47f7/7643467/a0d134d209b4/13287_2020_1985_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47f7/7643467/ca77e76bdbcb/13287_2020_1985_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47f7/7643467/d75270dcd9b2/13287_2020_1985_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47f7/7643467/f776ae9e4413/13287_2020_1985_Fig8_HTML.jpg

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