Anti-asialo GM1 antiserum treatment of lethally irradiated recipients before bone marrow transplantation: evidence that recipient natural killer depletion enhances survival, engraftment, and hematopoietic recovery
Anti-asialo GM1 antiserum treatment of lethally irradiated recipients before bone marrow transplantation: evidence that recipient natural killer depletion enhances survival, engraftment, and hematopoietic recovery
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骨髓移植前接受致命辐射的受者的抗去唾液酸 GM1 抗血清治疗：证据表明受者自然杀伤细胞耗竭可增强存活、植入和造血恢复
DOI：
10.1182/blood.v76.7.1419.bloodjournal7671419
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发表时间：
1990
期刊：
影响因子：
20.3
通讯作者：
Craig W. Reynolds
中科院分区：
文献类型：
--
作者：
P. Tiberghien;D. Longo;J. Wine;W. Alvord;Craig W. Reynolds
遗传控制的多态性细胞表面决定因素。 BMT 后 2 个月对存活动物的嵌合现象进行分析表明，受体 NK 自然杀伤 (NK) 细胞在骨髓 T 移植 (BMT) 中的作用先前已在各种不同的实验中进行了研究。多条证据表明，受体 NK 细胞对 BMT 后的造血重建具有有害影响，并且可能涉及至少两种不同的机制。 NK 细胞对 BMT 抵抗的一种机制被称为混合抵抗，源自观察到某些 F1 杂交小鼠可以拒绝来自父母的骨髓 (BM)，尽管它们会接受其他非淋巴组织^.^-^ 混合抵抗被认为是通过非共显性造血组织相容性 (Hh) 基因来调节的，并且因为介导这种抵抗的细胞似乎与具有 NK 活性的细胞共享许多特性，因此很可能杂交抗性和 NK 活性是由相同的细胞介导的。’。’杂交抗性和 NK 活性都处于相似的遗传控制之下”，并且通过识别大颗粒淋巴细胞 (LGL) 的抗血清处理在体内消除。2-4 亲代 BMT 的这种不寻常行为进一步扩展到同种异体和异种 BM 细胞的移植，”-’4 现在统称为遗传或造血抗性！最近，已经描述了与 NK 细胞对 BM 细胞生长或分化的正常稳态调节相关的第二种机制。在人类中，具有 NK 活性的 Percoll 梯度富集 LGL 可以在体外抑制自体或同种异体 BM 粒细胞-巨噬细胞集落的发育。I5 这些相同的细胞也抑制自体红细胞集落的发育。 l6 此外，具有 NK 活性的人类淋巴细胞克隆也已被证明能够以异质但克隆稳定的方式抑制体外造血。”一位患有再生障碍性贫血且多次同基因移植失败的患者提示，人类 NK 细胞可能在体内针对同基因细胞发挥作用，体外研究显示，当移植高剂量的 BM 时，供体的移植水平显着增加。这些研究还表明，抗ASGM1预处理主要导致照射后第二周和第三周髓外造血的增加。抗 ASGMI 治疗还显着加快了供体来源细胞的出现速度，当 NK 耗尽的和对照 BMT 受体之间的生存差异变得显着时，供体细胞植入水平明显提高。外周细胞计数也受到 NK 消耗的影响，血小板和红细胞恢复显着增强，粒细胞恢复适度增加。抗 ASGM1 受体治疗对 BMT 后造血事件的总体有利影响表明。在人类中，应评估旨在消除 NK 的移植前治疗方案。这是美国政府的工作。其使用没有任何限制。
of genetically controlled polymorphic cell surface determinants. Analysis of chimerism in surviving animals 2 months post-BMT showed that recipient NK HE ROLE OF natural killer (NK) cells in bone marrow T transplantation (BMT) has been previously studied in a variety of different experimental Several lines of evidence suggest that recipient NK cells have a deleterious effect on hematopoietic reconstitution after BMT, and that at least two different mechanisms could be involved. One mechanism of BMT resistance by NK cells has been termed hybrid resistance, and derives from the observation that certain F1 hybrid mice could reject bone marrow (BM) from their parents, although they would accept other nonlymphoid tissue^.^-^ Hybrid resistance is thought to be regulated through noncodominant hematopoietic-histocompatibility (Hh) genes,’ and because the cells that mediate this resistance appear to share a number of properties with cells having NK activity, it is likely that hybrid resistance and NK activity are mediated by the same cells.’.’ Both hybrid resistance and NK activity are under similar genetic control” and are abrogated in vivo by treatment with antisera recognizing large granular lymphocytes (LGL).2-4 This unusual behavior of parental BMT was further extended to the transplantation of allogeneic and xenogeneic BM cells,”-’4 and is now collectively termed genetic or hematopoietic resistance! More recently, a second mechanism related to the normal homeostatic regulation of BM cell growth or differentiation by NK cells has been described.’ In humans, Percoll gradientenriched LGL with NK activity can inhibit in vitro the development of granulocyte-macrophage colonies from either autologous or allogeneic BM.I5 These same cells also suppress the development of autologous erythrocyte colonies. l6 In addition, clones of human lymphocytes with NK activity have also been shown to suppress in vitro hematopoiesis in a heterogeneous but clonally stable manner.” The possibility that human NK cells might act in vivo against syngeneic cells has been suggested from a patient with aplastic anemia with repeated syngeneic graft failures, where in vitro studies depletion significantly increased the level of donor engraftment when high doses of BM were transplanted. These studies also demonstrated that anti-ASGM1 pretreatment mainly resulted in an increase in extramedullary hematopoiesis in the second and third week after irradiation. Anti-ASGMI treatment also dramatically accelerated the rate of appearance of donor-derived cells with a higher level of donor-cell engraftment apparent at a time when the differences in survival between NK-depleted and control BMT recipients became significant. Peripheral cell counts were also affected by NK depletion, with significantly enhanced platelet and red blood cell recovery and a moderate increase in granulocyte recovery. The overall favorable influence of anti-ASGM1 recipient treatment on hematopoietic events post-BMT suggests that. in humans, pretransplant regimens aimed toward NK depletion should be evaluated. This is a US government work. There are no restrictions on its use.
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对骨髓移植的自然抵抗的早期事件。
影响因子：
6.2
作者：
Carlson,GA;Marshall,ST;Kiesche,A
通讯作者：
Kiesche,A
T 淋巴细胞和自然杀伤细胞对造血的调节。
DOI：
10.1016/s1040-8428(87)80009-4
发表时间：
1987
期刊：
Critical reviews in oncology/hematology
影响因子：
--
作者：
Trinchieri,G;Murphy,M;Perussia,B
通讯作者：
Perussia,B
自我更新正常或减弱的多能干细胞在致命辐射下仍能存活。
影响因子：
2.6
作者：
Brecher,G;Neben,S;Yee,M;Bullis,J;Cronkite,EP
通讯作者：
Cronkite,EP
自然杀伤细胞对人类造血作用的体外调节：克隆水平的分析。
影响因子：
20.3
作者：
Herrmann,F;Schmidt,RE;Ritz,J;Griffin,JD
通讯作者：
Griffin,JD
自然杀伤细胞在体外抑制人红细胞干细胞增殖。
影响因子：
20.3
作者：
Mangan,KF;Hartnett,ME;Matis,SA;Winkelstein,A;Abo,T
通讯作者：
Abo,T