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体内给予重组 BTNL2-Fc 融合蛋白可改善小鼠移植物抗宿主病。

In vivo administration of recombinant BTNL2-Fc fusion protein ameliorates graft-versus-host disease in mice.

机构信息

Department of Allied Health Sciences, University of Connecticut, Storrs, CT, United States; Department of Physiology, College of Basic Medical Science, China Medical University, Shenyang, Liaoning, China.

Department of Allied Health Sciences, University of Connecticut, Storrs, CT, United States.

出版信息

Cell Immunol. 2019 Jan;335:22-29. doi: 10.1016/j.cellimm.2018.10.008. Epub 2018 Oct 26.

DOI:10.1016/j.cellimm.2018.10.008
PMID:30389093
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6368466/
Abstract

Although hematopoietic stem cell transplantation (HSCT) has been widely used in the treatment of many diseases, graft-versus-host disease (GVHD) remains a major complication after allogeneic HSCT. Butyrophilin-like 2 (BTNL2) protein has been reported to have the ability to inhibit T cell proliferation in vitro; its ability to inhibit T cell responses in vivo has not been determined. We show here that in vivo administration of recombinant BTNL2-IgG2a Fc (rBTNL2-Ig) fusion protein ameliorates GVHD in mice. This is related to the ability of rBTNL2-Ig to inhibit T cell proliferation, activation and Th1/Th17 cytokine production in vivo. Furthermore, rBTNL2-Ig treatment increases the generation of regulatory T cells. Our results suggest that rBTNL2-Ig has the potential to be used in the prevention and treatment of patients with GVHD.

摘要

虽然造血干细胞移植(HSCT)已被广泛应用于治疗多种疾病,但移植物抗宿主病(GVHD)仍然是异基因 HSCT 后的主要并发症。有报道称,BTNL2 样蛋白 2(BTNL2)具有体外抑制 T 细胞增殖的能力,但它在体内抑制 T 细胞反应的能力尚未确定。我们在这里表明,体内给予重组 BTNL2-IgG2a Fc(rBTNL2-Ig)融合蛋白可改善小鼠的 GVHD。这与 rBTNL2-Ig 抑制 T 细胞增殖、体内 T 细胞活化和 Th1/Th17 细胞因子产生的能力有关。此外,rBTNL2-Ig 治疗可增加调节性 T 细胞的产生。我们的研究结果表明,rBTNL2-Ig 有可能用于预防和治疗 GVHD 患者。

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本文引用的文献

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