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在狼疮样移植物抗宿主病中,同种异体辅助性T细胞的持续存在是维持自身抗体形成所必需的。

Persistence of allospecific helper T cells is required for maintaining autoantibody formation in lupus-like graft-versus-host disease.

作者信息

Rozendaal L, Pals S T, Gleichmann E, Melief C J

机构信息

Central Laboratory of The Netherlands Red Cross Blood Transfusion Service, Amsterdam.

出版信息

Clin Exp Immunol. 1990 Dec;82(3):527-32. doi: 10.1111/j.1365-2249.1990.tb05484.x.

Abstract

Induction of a graft-versus-host (GVH) reaction (GVHR) in non-irradiated (C57BL/10ScSn x DBA/2)F1 mice (BDF1) with DBA/2 lymphoid cells leads to chronic GVH disease (GVHD). One of the pathological alterations of this type of GVHD is hyperplasia of host B cells with production of lupus-like autoantibodies. This hyperstimulation of host B cells has previously been demonstrated to be induced by alloreactive donor T helper cells that were also proposed to maintain it. We provide three pieces of experimental evidence in support of this concept. First, treatment of mice with chronic GVHD by injection of monoclonal anti-Thy-1.2 antibodies, performed at week 6 after the injection of C57BL/6 lymphoid cells into (C57BL/6 x C57BL.bm12)F1 mice led to a significant decrease in the titre of anti-nuclear antibodies. Second, CD4+ donor T cells persisted in BDF1 mice with GVHD (GVHF1) for at least 10 weeks after the induction of GVHR; these T cells showed alloreactive helper activity against H-2b MHC determinants of the opposite parent in vitro. Third, T cells of GVHF1 mice, obtained 2 months after the induction of GVHR and transferred into normal secondary recipients, induced signs of chronic GVHD in DBF1 but not in DBA/2 mice. The combined results show that persisting donor T helper cells in GVHF1 mice retain their alloreactivity towards H-2 class II antigens for a long time after the induction of GVHR and they strongly suggest that these T cells are also the driving force behind the production of lupus-like autoantibodies at the late stage of chronic GVHD.

摘要

用DBA/2淋巴细胞在未受照射的(C57BL/10ScSn×DBA/2)F1小鼠(BDF1)中诱导移植物抗宿主(GVH)反应(GVHR)会导致慢性移植物抗宿主病(GVHD)。这类GVHD的病理改变之一是宿主B细胞增生并产生狼疮样自身抗体。此前已证明,宿主B细胞的这种过度刺激是由同种反应性供体T辅助细胞诱导的,也有人提出这些T辅助细胞维持了这种刺激。我们提供了三条实验证据来支持这一概念。第一,在将C57BL/6淋巴细胞注射到(C57BL/6×C57BL.bm12)F1小鼠后第6周,通过注射单克隆抗Thy-1.2抗体治疗患有慢性GVHD的小鼠,结果抗核抗体滴度显著降低。第二,在GVHR诱导后,CD4⁺供体T细胞在患有GVHD的BDF1小鼠(GVHF1)中持续存在至少10周;这些T细胞在体外对另一亲本的H-2b MHC决定簇表现出同种反应性辅助活性。第三,在GVHR诱导2个月后从小鼠GVHF1获得的T细胞,转移到正常二级受体中,在DBF1小鼠中诱导出慢性GVHD的迹象,但在DBA/2小鼠中未诱导出。综合结果表明,GVHF1小鼠中持续存在的供体T辅助细胞在GVHR诱导后很长时间内仍对H-2Ⅱ类抗原保持同种反应性,并且强烈表明这些T细胞也是慢性GVHD晚期狼疮样自身抗体产生的驱动力。

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