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骨髓移植后，细胞内源性 Th2 途径促进受者 T 淋巴细胞存活并调节移植物抗宿主病。

After Bone Marrow Transplantation, the Cell-Intrinsic Th2 Pathway Promotes Recipient T Lymphocyte Survival and Regulates Graft-versus-Host Disease.

机构信息

Department of Pediatrics, Carver College of Medicine, University of Iowa, Iowa City, IA.

Department of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City, IA.

出版信息

Immunohorizons. 2023 Jun 1;7(6):442-455. doi: 10.4049/immunohorizons.2300021.

DOI:10.4049/immunohorizons.2300021
PMID:37294277
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10580113/
Abstract

Recipient T cells can aggravate or regulate lethal and devastating graft-versus-host disease (GVHD) after bone marrow transplantation (BMT). In this context, we have shown before that intestinal immune conditioning with helminths is associated with survival of recipient T cells and Th2 pathway-dependent regulation of GVHD. We investigated the mechanism of survival of recipient T cells and their contribution to GVHD pathogenesis in this helminth infection and BMT model after myeloablative preparation with total body irradiation in mice. Our results indicate that the helminth-induced Th2 pathway directly promotes the survival of recipient T cells after total body irradiation. Th2 cells also directly stimulate recipient T cells to produce TGF-β, which is required to regulate donor T cell-mediated immune attack of GVHD and can thereby contribute to recipient T cell survival after BMT. Moreover, we show that recipient T cells, conditioned to produce Th2 cytokines and TGF-β after helminth infection, are fundamentally necessary for GVHD regulation. Taken together, reprogrammed or immune-conditioned recipient T cells after helminth infection are crucial elements of Th2- and TGF-β-dependent regulation of GVHD after BMT, and their survival is dependent on cell-intrinsic Th2 signaling.

摘要

受者 T 细胞在骨髓移植（BMT）后可加重或调节致命性和破坏性移植物抗宿主病（GVHD）。在此背景下，我们之前已经证明，用寄生虫进行肠道免疫调理与受者 T 细胞的存活以及 GVHD 的 Th2 通路依赖性调节有关。我们在经过全身照射的骨髓清除性准备后，在寄生虫感染和 BMT 模型中研究了受者 T 细胞存活的机制及其对 GVHD 发病机制的贡献。我们的结果表明，寄生虫诱导的 Th2 通路直接促进了全身照射后受者 T 细胞的存活。Th2 细胞还直接刺激受者 T 细胞产生 TGF-β，这是调节供者 T 细胞介导的 GVHD 免疫攻击所必需的，从而有助于 BMT 后受者 T 细胞的存活。此外，我们还表明，在寄生虫感染后产生 Th2 细胞因子和 TGF-β的受者 T 细胞对于 GVHD 的调节是根本必需的。总之，寄生虫感染后重编程或免疫调理的受者 T 细胞是 BMT 后 Th2 和 TGF-β依赖性 GVHD 调节的关键因素，其存活依赖于细胞内在的 Th2 信号。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e7f/10580113/73bd43e00868/ih2300021f9.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e7f/10580113/73bd43e00868/ih2300021f9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e7f/10580113/ca6b40c990e3/ih2300021f1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e7f/10580113/1f8a2920acd4/ih2300021f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e7f/10580113/ecf13c7fc099/ih2300021f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e7f/10580113/73bd43e00868/ih2300021f9.jpg

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