Loughran T P, Starkebaum G, Aprile J A
Fred Hutchinson Cancer Research Center, Department of Medicine, University of Washington School of Medicine, Seattle 98104.
Blood. 1988 Mar;71(3):822-4.
Ten patients with large granular lymphocyte (LGL) leukemia were studied for rearrangement and expression of T cell receptor (TCR) genes. Eight patients with CD3+ LGL proliferation had unique TCR beta-gene rearrangements, supporting a clonal process. Each of five patients studied with CD3+ disease had evidence for expression of full-length TCR alpha-, beta-, and gamma-gene transcripts. In contrast, patients with CD3- LGL proliferation had no evidence for rearrangement or expression of TCR genes. These studies suggest that leukemic LGL arise from two different cell origins. Leukemic LGL may be a useful model for studying natural killer (NK) cell (CD3- LGL) and non-MHC-restricted cytotoxic T lymphocyte (CD3+ LGL) activation and differentiation.
对10例大颗粒淋巴细胞（LGL）白血病患者进行了T细胞受体（TCR）基因重排和表达研究。8例CD3⁺ LGL增殖患者有独特的TCRβ基因重排，支持克隆性过程。研究的5例CD3⁺疾病患者均有全长TCRα、β和γ基因转录本表达的证据。相比之下，CD3⁻ LGL增殖患者没有TCR基因重排或表达的证据。这些研究表明，白血病性LGL起源于两种不同的细胞来源。白血病性LGL可能是研究自然杀伤（NK）细胞（CD3⁻ LGL）和非MHC限制性细胞毒性T淋巴细胞（CD3⁺ LGL）活化与分化的有用模型。
