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Thy1+骨髓细胞调节小鼠同基因移植物抗宿主病的诱导。

Thy1+ bone marrow cells regulate the induction of murine syngeneic graft-versus-host disease.

作者信息

Bryson J S, Jennings C D, Caywood B E, Kaplan A M

机构信息

Department of Microbiology and Immunology, College of Medicine, Chandler Medical Center, University of Kentucky, Lexington 40536-0084.

出版信息

Transplantation. 1993 Oct;56(4):941-5. doi: 10.1097/00007890-199310000-00031.

Abstract

A syngeneic graft-versus-host disease (GVHD)-like syndrome has been shown to be inducible in some strains of mice after lethal irradiation, reconstitution with syngeneic bone marrow (BM), and treatment with a short course of CsA therapy. Since Thy1+ BM cells have been shown to regulate the development of other experimental autoimmune diseases, it was important to determine their role in the inducibility of syngeneic GVHD (SGVHD) in different strains of mice. Lethally irradiated mice were reconstituted with either syngeneic BM or T cell-depleted syngeneic BM, then treated with CsA or diluent. Removal of Thy1+ cells from BM before reconstitution of an inducible strain, C3H/HeN, exacerbated SGVHD when compared with animals given whole BM cells before CsA treatment. Furthermore, a noninducible strain, C57BL/6 mice, developed SGVHD when reconstituted with T cell-depleted syngeneic BM but not BM before CsA therapy. These results suggest that Thy1+ BM cells may regulate the development of SGVHD, and be of importance in controlling autoreactivity after bone marrow transplantation.

摘要

在致死性照射、同基因骨髓(BM)重建以及短期环孢素A(CsA)治疗后,已证实在某些品系小鼠中可诱导出同基因移植物抗宿主病(GVHD)样综合征。由于已表明Thy1⁺ BM细胞可调节其他实验性自身免疫性疾病的发展,因此确定它们在不同品系小鼠同基因GVHD(SGVHD)诱导中的作用很重要。对致死性照射的小鼠用同基因BM或去除T细胞的同基因BM进行重建,然后用CsA或稀释剂处理。在可诱导品系C3H/HeN重建前从BM中去除Thy1⁺细胞,与在CsA治疗前给予全BM细胞的动物相比,会加剧SGVHD。此外,不可诱导品系C57BL/6小鼠在用去除T细胞的同基因BM重建时会发生SGVHD,但在CsA治疗前用BM重建则不会。这些结果表明,Thy1⁺ BM细胞可能调节SGVHD的发展,并且在控制骨髓移植后的自身反应性方面具有重要意义。

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