Naumovski L, Utz P J, Bergstrom S K, Morgan R, Molina A, Toole J J, Glader B E, McFall P, Weiss L M, Warnke R
Department of Pediatrics, Stanford University School of Medicine, CA.
Blood. 1989 Dec;74(8):2733-42.
A new cell line, SUP-HD1, was established from the pleural effusion of a patient with nodular sclerosing Hodgkin's disease (NSHD). The SUP-HD1 cells had the characteristic morphology of Reed-Sternberg cells and contained acid phosphatase and nonspecific esterase. The cells lacked the Epstein-Barr virus (EBV) genome and reacted with monoclonal antibodies (MoAbs) against CD15 (Leu-M1), CD25 (Tac), CD71 (OKT9), Ki67, and HLA-Dr. However, the SUP-HD1 cells were nonreactive with MoAbs that specifically identify T lymphocytes, B lymphocytes, and macrophage/myeloid cells. Karyotype analysis of the cell line showed clonal abnormalities involving 1p13, 7p15, 8q22, and 11q23, chromosomal locations, at which breakpoints have been reported in HD. Southern blot analysis demonstrated rearrangement of the immunoglobulin heavy chain and kappa light chain genes as well as the gene for the beta chain of the T-cell receptor (TCR). Transcriptional analysis showed expression of RNAs for kappa light chain, interferon-gamma (IFN-gamma), and interleukin-2 receptor (IL-2R) but not IL-2. The SUP-HD1 cells lacked cytoplasmic and surface immunoglobulin heavy chain, but a small amount of cytoplasmic kappa light chain was detected. The presence of nuclear factor kappa B (NF kappa B), a B-lymphocyte-associated transcription factor, was demonstrated in stimulated and unstimulated cells. In addition, the SUP-HD1 cell line, produced IFN-gamma, a T-lymphocyte-associated lymphokine. Based on these data, the SUP-HD1 cells appear to be aberrant lymphocytes with characteristics of both activated B and T lymphocytes. Elaboration of lymphokines such as IFN-gamma by the malignant cells may represent one explanation for the unique clinical and pathologic features of HD.
一种新的细胞系SUP - HD1，是从一名结节硬化型霍奇金病（NSHD）患者的胸腔积液中建立的。SUP - HD1细胞具有里德 - 斯腾伯格细胞的特征形态，并且含有酸性磷酸酶和非特异性酯酶。这些细胞缺乏爱泼斯坦 - 巴尔病毒（EBV）基因组，并与抗CD15（Leu - M1）、CD25（Tac）、CD71（OKT9）、Ki67和HLA - Dr的单克隆抗体（MoAbs）发生反应。然而，SUP - HD1细胞与特异性识别T淋巴细胞、B淋巴细胞以及巨噬细胞/髓样细胞的MoAbs无反应。对该细胞系的核型分析显示存在涉及1p13、7p15、8q22和11q23的克隆异常，这些染色体位置在霍奇金病中已有断点报道。Southern印迹分析表明免疫球蛋白重链和κ轻链基因以及T细胞受体（TCR）β链基因发生了重排。转录分析显示κ轻链、干扰素 - γ（IFN - γ）和白细胞介素 - 2受体（IL - 2R）的RNA有表达，但IL - 2无表达。SUP - HD1细胞缺乏细胞质和表面免疫球蛋白重链，但检测到少量细胞质κ轻链。在刺激和未刺激的细胞中均证实存在核因子κB（NFκB），一种B淋巴细胞相关的转录因子。此外，SUP - HD1细胞系产生IFN - γ，一种T淋巴细胞相关的淋巴因子。基于这些数据，SUP - HD1细胞似乎是具有活化B和T淋巴细胞特征的异常淋巴细胞。恶性细胞产生如IFN - γ等淋巴因子可能是霍奇金病独特临床和病理特征的一种解释。
