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分化早期小儿急性白血病细胞免疫球蛋白和T细胞受体基因结构的变化 被引量:3

Alteration of configuration of immunoglobulin and T cell receptor genes in early stage of children acute leukemia
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摘要 从29例免疫分型的小儿急性白血病中选出髓过氧化物酶染色阴性和不与细胞系相关或成熟细胞系相关的单克隆抗体反应的6例白血病细胞,进一步作免疫球蛋白(包括重链和κ轻链)和T细胞受体(包括δ、γ、β)基因结构的分析。所有6例均有IgH基因的重排,提示这些白血病细胞是β细胞来源。两例CD_(10)阴性和白病细胞.κ链基因没有重排,其中一例的TCRδ、γ、β基因也都处于胚系,另一例的TCRβ处于胚系。在CD_(10)阳性白血病细胞中,其中两例κ链基因丢失,TCR基因结构都有不同程度的变化(重排或丢失)。这些结果可能提示在CD_(10)阳性白血病细胞中能产生功能性IgH的重排,并可导致IgL和TCR基因结构的变化。 Phenotypic markers of leukemic cells from 29 children with acute leukemia were examined. Of these cases, six were negative for myeloperoxidase and did not react with lineage-associated or mature lineage-associated monoclonal antibodies. Then, we analyzed the configuration of both immunoglobulin (heavy chain and kappa chain) and T-cell receptor (δ, γ, β) genes in these six cases. All cases had rearrangement of IgH were suggestive of B-lymphoid origin of these leukemic cells. Two cases without CD10 antigen had no rearrangement of kappa chain, one with retention of the germline configuration of TCR δ, γ. β, the other with retention of the germline of TCR β gene. In the cases with CD10 antigen, two cases showed kappa chain deletion, the alteration of TCR genes (rearrangements or deletions )was shown to occur frequently. These findings may implicate that the gene rearrange ments forming functional IgH gene in leukemic cells with CD10 antigen, induce the alteration of IgL and TCR genes.
出处 《中国免疫学杂志》 CAS CSCD 北大核心 1991年第2期79-84,共6页 Chinese Journal of Immunology
基金 国家自然科学基金
关键词 白血病 免疫球蛋白 T细胞受体 Immunoglobulin gene T-cell receptor gene Immnoglobulin gene rearrangement and deletion TCR gene rearrangement and deletion Children acute leukemia
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同被引文献16

  • 1余英豪,朱梅刚,季卉,赵彤,张素娟,吴秋良.聚合酶链反应扩增T细胞受体β基因重排在检测T细胞淋巴瘤克隆中的应用[J].中华血液学杂志,1994,15(4):203-204. 被引量:2
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  • 10Loiseau P,Guglielmi P,Le Paslier D et al.Rearrangement of the T cell receptor δ gene in T acute lymphoblastic leukemia cells are distinct from those occuring in B lineage acute lymphoblastic leukemia and preferentially involve one Vδgene segment. J Immunol . 1989

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