Wang L, Tadokoro K, Tokunaga K, Uchida S, Moriyama S, Bannai M, Mitsunaga S, Takai K, Juji T
Department of Research, Japanese Red Cross Central Blood Center, Tokyo.
Transfusion. 1997 Nov-Dec;37(11-12):1184-91. doi: 10.1046/j.1537-2995.1997.37111298088050.x.
Posttransfusion graft-versus-host disease (PT-GVHD) is a pathophysiological process of the immune system. Mature donor T cells that have survived the host defense mechanisms recognize recipient allo-antigens through antigen-specific T-cell receptors and mount an immune attack against certain host antigens.
To characterize the T cells involved in PT-GVHD, expression of the T-cell receptor V beta genes in peripheral blood T cells isolated from four PT-GVHD patients was analyzed. T-cell receptor beta chain cDNA derived from mRNA extracted from peripheral blood lymphocytes was amplified by an inverse polymerase chain reaction method, and the cDNA was subsequently cloned and sequenced.
The cDNA clones derived from patients with PT-GVHD showed remarkable differences in the distribution of T-cell receptor V beta gene use from that in normal controls. Very restricted T-cell receptor V beta gene repertoires and preferential expression of certain V beta gene segments were revealed in the peripheral blood lymphocytes of each patients. Shared V beta gene use among the patients was not observed, probably because of HLA differences among the patient-donor combinations.
This restricted use reflected in vivo expansion of a limited number of engrafted T-cell clones at the onset of PT-GVHD and suggested that those oligoclonal donor T cells may be involved in the induction of PT-GVHD.
输血后移植物抗宿主病(PT-GVHD)是一种免疫系统的病理生理过程。在宿主防御机制中存活下来的成熟供体T细胞通过抗原特异性T细胞受体识别受体同种异体抗原,并对某些宿主抗原发动免疫攻击。
为了表征参与PT-GVHD的T细胞,分析了从4例PT-GVHD患者分离的外周血T细胞中T细胞受体Vβ基因的表达。通过逆转录聚合酶链反应方法扩增从外周血淋巴细胞提取的mRNA衍生的T细胞受体β链cDNA,随后对该cDNA进行克隆和测序。
PT-GVHD患者来源的cDNA克隆在T细胞受体Vβ基因使用分布上与正常对照有显著差异。在每位患者的外周血淋巴细胞中均显示出非常有限的T细胞受体Vβ基因库以及某些Vβ基因片段的优先表达。未观察到患者之间共享的Vβ基因使用情况,这可能是由于患者-供体组合之间的HLA差异所致。
这种有限的使用反映了PT-GVHD发病时有限数量的植入T细胞克隆在体内的扩增,并表明那些寡克隆供体T细胞可能参与了PT-GVHD的诱导。