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小鼠移植物抗宿主诱导的淋巴结病机制。滞留与增殖。

Mechanism of graft-versus-host-induced lymphadenopathy in mice. Trapping vs. proliferation.

作者信息

Emeson E E, Thursh D R

出版信息

J Exp Med. 1973 May 1;137(5):1293-302. doi: 10.1084/jem.137.5.1293.

Abstract

Graft-vs.-host (GVH)-induced lymphadenopathy of the popliteal lymph node has been produced in C57BL/6 x A/J F(1) (BAF(1)) mice by injecting A/J spleen cells into the rear footpads. By giving (51)Cr-labeled BAF(1) lymphoid cells intravenously to the hosts, 24 h before sacrifice, we have demonstrated that a large portion of the GVH-induced lymphadenopathy is due to the trapping of circuating lymphocytes in the challenged lymph nodes. Most of the remaining enlargement can be attributed to proliferation of host cells within the reacting lymph nodes. Conditions have been defined under which the weights and [(14)C]thymidine incorporation of the popliteal nodes can be plotted against the dose of injected A/J spleen cells on a double-log scale to give a linear dose-response. The popliteal lymph node GVH assay is a simple and effective means of quantitating immune reactivity to histocompatibility antigens in mice.

摘要

通过将A/J脾细胞注射到C57BL/6×A/J F(1)(BAF(1))小鼠的后足垫中,已在这些小鼠中诱发了移植物抗宿主(GVH)诱导的腘淋巴结病。在处死宿主前24小时,通过给宿主静脉注射(51)Cr标记的BAF(1)淋巴细胞,我们已证明大部分GVH诱导的淋巴结病是由于循环淋巴细胞在受攻击的淋巴结中滞留所致。其余大部分肿大可归因于反应性淋巴结内宿主细胞的增殖。已确定了相关条件,在此条件下,腘淋巴结的重量和[(14)C]胸苷掺入量可以在双对数尺度上相对于注射的A/J脾细胞剂量作图,以给出线性剂量反应。腘淋巴结GVH测定是定量小鼠对组织相容性抗原免疫反应性的一种简单而有效的方法。

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