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在无可检测到的细胞毒性T淋巴细胞的情况下发生的致死性小鼠移植物抗宿主病。

Lethal murine graft-versus-host disease in the absence of detectable cytotoxic T lymphocytes.

作者信息

Jadus M R, Peck A B

出版信息

Transplantation. 1983 Sep;36(3):281-9. doi: 10.1097/00007890-198309000-00011.

DOI:10.1097/00007890-198309000-00011
PMID:6604351
Abstract

The cytotoxic reactivity of cells recovered from host organs undergoing severe graft-versus-host (GVH) reactivity resulting from donor-recipient histoincompatibility at the entire H-2 complex, the H-2 I region alone, or the H-2 K/D regions have been examined. In all H-2 or H-2 I-region-disparate combinations acute lethal GVH disease occurred. In H-2-K/D-region-disparate combinations mortality was only 60-80%; however, injections of Interleukin-2 increased mortality to 100%. Donor antihost cytotoxic lymphocytes (CTLs) could be recovered from the organs and tissues of GVH animals mismatched at the entire H-2 complex or K/D mismatches but not from animals mismatched at only the I regions. In K/D region mismatches, only a weak transient antihost CTL response was detected. In the I region mismatches, antidonor cytotoxic reactivity appeared most frequently and could be expanded in vitro using Interleukin-2 (IL-2). In addition, lethal GVH disease was induced in hosts with cloned anti-I-A, Lyt-1+ noncytotoxic T helper cells. Thus, if CTLs or T suppressor cells are essential for the development of lethal GVH disease, they must be derived from the host per se. We conclude, therefore, that there is no absolute correlation between lethal GVH and the development of donor-derived CTLs or T suppressor cells.

摘要

对从因供体 - 受体在整个H - 2复合体、仅H - 2 I区或H - 2 K/D区存在组织相容性差异而发生严重移植物抗宿主(GVH)反应的宿主器官中回收的细胞的细胞毒性反应性进行了检测。在所有H - 2或H - 2 I区不同的组合中,均发生了急性致死性GVH病。在H - 2 K/D区不同的组合中,死亡率仅为60% - 80%;然而,注射白细胞介素 - 2可使死亡率增至100%。供体抗宿主细胞毒性淋巴细胞(CTLs)可从在整个H - 2复合体不匹配或K/D不匹配的GVH动物的器官和组织中回收,但不能从仅在I区不匹配的动物中回收。在K/D区不匹配中,仅检测到微弱的短暂抗宿主CTL反应。在I区不匹配中,抗供体细胞毒性反应最常出现,并且可用白细胞介素 - 2(IL - 2)在体外扩增。此外,用克隆的抗I - A、Lyt - 1 + 无细胞毒性T辅助细胞可在宿主中诱导致死性GVH病。因此,如果CTLs或T抑制细胞对致死性GVH病的发生至关重要,那么它们必定源自宿主本身。所以,我们得出结论,致死性GVH与供体来源的CTLs或T抑制细胞的发生之间不存在绝对的相关性。

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Lethal murine graft-versus-host disease in the absence of detectable cytotoxic T lymphocytes.在无可检测到的细胞毒性T淋巴细胞的情况下发生的致死性小鼠移植物抗宿主病。
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引用本文的文献

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Study of relieving graft-versus-host disease by blocking CD137-CD137 ligand costimulatory pathway in vitro.体外阻断CD137-CD137配体共刺激通路缓解移植物抗宿主病的研究
Int J Hematol. 2007 Jul;86(1):84-90. doi: 10.1532/IJH97.A10613.
2
Graft-versus-host disease and the Th1/Th2 paradigm.移植物抗宿主病与Th1/Th2范式
Immunol Res. 1996;15(1):50-73. doi: 10.1007/BF02918284.
3
Variable capacity of L3T4+ T cells to cause lethal graft-versus-host disease across minor histocompatibility barriers in mice.L3T4+ T细胞在跨越小鼠次要组织相容性屏障时引发致死性移植物抗宿主病的能力存在差异。
J Exp Med. 1987 Jun 1;165(6):1552-64. doi: 10.1084/jem.165.6.1552.
4
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J Exp Med. 1988 Feb 1;167(2):556-69. doi: 10.1084/jem.167.2.556.
5
In vivo administration of interleukin 2 plus T cell-depleted syngeneic marrow prevents graft-versus-host disease mortality and permits alloengraftment.体内给予白细胞介素2加去除T细胞的同基因骨髓可预防移植物抗宿主病死亡并允许同种异体移植。
J Exp Med. 1990 Mar 1;171(3):645-58. doi: 10.1084/jem.171.3.645.
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Specific eradication of micrometastases by transfer of tumour-immune T cells from major-histocompatibility-complex congenic mice.通过移植来自主要组织相容性复合体同基因小鼠的肿瘤免疫T细胞特异性根除微转移灶。
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