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供体与宿主淋巴细胞在局部移植物抗宿主反应诱导的肾皮质破坏发病机制中的相互作用。

The interaction of donor and host lymphoid cells in the pathogenesis of renal cortical destruction induced by a local graft versus host reaction.

作者信息

Elkins W L

出版信息

J Exp Med. 1966 Jan 1;123(1):103-18. doi: 10.1084/jem.123.1.103.

Abstract

The graft versus host reaction (GVHR), which results from the injection of parental strain spleen cells beneath the kidney capsule of F(1) hybrid rats, is transferable during its developmental phase into F(1) hybrid hosts isogeneic with the primary host, but not into secondary hosts of the parental (donor) strain. Furthermore, the GVHR propagates but rarely in secondary hybrid hosts which are allogeneic with respect to the primary hosts, but which are also genetically tolerant of donor-type cells. These findings indicate that the donor cells not only initiate the GVHR but also maintain it by virtue of immunologically specific activity. Whole-body irradiation of (LBf)F(1) and (LBN)F(1) hosts 24 hours prior to the injection of parental (L) spleen cells results in inhibition of the subsequent GVHR to a degree commensurate with the radiation damage sustained by the lymphoid system of the host. Furthermore, propagation of transferred GVHRs did not occur if susceptible secondary hybrid hosts had been previously irradiated. These findings indicate that radiosensitive host cells play a continuing and essential role in the pathogenesis of the invasive-destructive lesion. It is concluded that the development of this lesion depends upon the continuous interaction of the specifically reactive donor-type cells with an immunologically non-specific population of host mononuclears.

摘要

移植物抗宿主反应(GVHR)是由将亲代品系脾细胞注射到F(1)杂种大鼠肾被膜下引发的。在其发育阶段,该反应可转移至与原宿主同基因的F(1)杂种宿主中,但不能转移至亲代(供体)品系的二级宿主中。此外,GVHR在与原宿主异基因但对供体类型细胞具有遗传耐受性的二级杂种宿主中很少传播。这些发现表明,供体细胞不仅启动了GVHR,还凭借免疫特异性活性维持该反应。在注射亲代(L)脾细胞前24小时,对(LBf)F(1)和(LBN)F(1)宿主进行全身照射,会导致随后的GVHR受到抑制,其程度与宿主淋巴系统所遭受的辐射损伤程度相当。此外,如果易感的二级杂种宿主先前已接受照射,则转移的GVHR不会传播。这些发现表明,对辐射敏感的宿主细胞在侵袭性破坏性病损的发病机制中持续发挥着重要作用。得出的结论是,这种病损的发展取决于具有特异性反应的供体类型细胞与宿主单核细胞的免疫非特异性群体之间的持续相互作用。

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