首页> 美国卫生研究院文献>The Journal of Experimental Medicine >Allosuppressor and allohelper T cells in acute and chronic graft-vs- host disease. V. F1 mice with secondary chronic GVHD contain F1- reactive allohelper but no allosuppressor T cells
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Allosuppressor and allohelper T cells in acute and chronic graft-vs- host disease. V. F1 mice with secondary chronic GVHD contain F1- reactive allohelper but no allosuppressor T cells

机译:急性和慢性移植物抗宿主病中的同种异体抑制剂和同种异体辅助性T细胞。 V.患有继发性慢性GVHD的F1小鼠含有F1反应性同种异体辅助物但没有同种异体抑制性T细胞

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摘要

We studied the alloreactive properties of donor T cells obtained from F1 mice that had recovered from the allosuppression of acute graft-vs.- host disease (GVHD) and showed mild symptoms of chronic GVHD, i.e., so- called secondary chronic GVHD. To this end, we used (B10 x DBA/2)F1 mice that had been injected with 10(8) B10 spleen cells 100-150 d previously. Such GVHD F1 mice were repopulated by lympho-hematopoietic cells of donor (B10) origin, which exhibited split tolerance towards the host: Whereas F1-specific donor T helper (Th) cells as well as T cells proliferating in the mixed lymphocyte reaction were readily demonstrable, F1-specific T suppressor (Ts) and T killer (Tk) cells were not, or were hardly, detectable; responses against third-party alloantigens were normal. Upon adoptive transfer to nonirradiated secondary recipients, the B10 cells obtained from the repopulated GVH F1 mice induced F1-specific enlargement of the draining popliteal lymph node and enhancement of the IgG formation therein. B10 cells of the same kind were unable, however, to induce lethal GVHD upon transfer to 950 rad-irradiated secondary (B10 x DBA/2)F1 recipients. We conclude that alloactivated donor Ts/Tk cells disappear from the host at a relatively early stage of GVHD, i.e., at the end of acute GVHD , presumably because they are short-lived. By contrast, the longevity of alloactivated donor Th cells causes the symptoms of secondary chronic GVHD.
机译:我们研究了从F1小鼠获得的供体T细胞的同种反应特性,这些F1小鼠已从急性移植物抗宿主病(GVHD)的同种异体抑制中恢复,并显示出慢性GVHD的轻度症状,即所谓的继发性慢性GVHD。为此,我们使用(B10 x DBA / 2)F1小鼠,这些小鼠先前已在100-150 d注射了10(8)个B10脾细胞。此类GVHD F1小鼠被供体(B10)来源的淋巴造血细胞再填充,该细胞对宿主表现出分裂耐受性:而F1特异性供体T辅助(Th)细胞以及在混合淋巴细胞反应中增殖的T细胞很容易可证实的是,F1特异性T抑制子(Ts)和T杀手(Tk)细胞无法或几乎无法检测到。对第三方同种异体抗原的反应正常。在过继转移至未辐照的次要受体后,从再填充的GVH F1小鼠获得的B10细胞诱导了引流pop部淋巴结的F1特异性扩增并增强了其中的IgG形成。但是,相同类型的B10细胞在转移至950辐射照射的次要(B10 x DBA / 2)F1受体后,无法诱导致死性GVHD。我们得出的结论是,同种激活的供体Ts / Tk细胞在相对较早的GVHD阶段即急性GVHD结束时从宿主中消失了,大概是因为它们的寿命很短。相反,同种激活的供体Th细胞的寿命会导致继发性慢性GVHD症状。

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