Semenzato G, Zambello R, Starkebaum G, Oshimi K, Loughran T P
Department of Clinical and Experimental Medicine, Padua University School of Medicine, Italy.
Blood. 1997 Jan 1;89(1):256-60.
The lymphoproliferative disease of granular lymphocytes (LDGL), also referred to as LGL leukemia, is a heterogeneous disorder, but is clinically, morphologically, and immunologically distinct. Although LDGL has recently been included in the revised classification of lymphomas as an independent clinical entity, no consensus exists on the criteria to establish the diagnosis. The aim of this report was to refine the parameters needed to make the diagnosis of LDGL. We studied 11 patients with chronic granular lymphocytosis selected from among 195 cases observed by our institutions from three different geographic areas (North America, Europe, and Asia). These cases did not meet the current criteria for inclusion in LDGL, since all patients had less than 2,000 GL/microL. However, in each of these patients, we found evidence for expansion of a discrete GL population. Clonal rearrangement of the T-cell receptor (TCR) beta gene was found in peripheral blood mononuclear cells (PBMC) of all nine patients with CD3+ LDGL. Using recently generated monoclonal antibodies (MoAbs) against the TCR V beta gene regions, we identified a unique TCR V beta on GL from each of three patients studied. In two patients with CD3- LDGL, we also identified a restricted pattern of reactivity, by staining with MoAbs against p58 antigen found on normal natural killer (NK) cells. The clinical features of these 11 patients with relatively low absolute number of GL were similar to those reported previously for patients with greater than 2,000 GL/microL. These data demonstrate that newer techniques such as MoAbs against V beta gene regions and p58 molecules and molecular analyses are useful to identify expansions of discrete GL proliferations. Demonstration of an expansion of a restricted GL subset is evidence for the diagnosis of LDGL, even in patients with a relatively low GL count. Our results also contribute to distinguish between the end of normality and the beginning of pathology in the broad spectrum of GL lymphocytoses.
颗粒淋巴细胞增殖性疾病(LDGL),也称为大颗粒淋巴细胞白血病,是一种异质性疾病,但在临床、形态学和免疫学上具有独特性。尽管LDGL最近已被纳入淋巴瘤修订分类中作为一个独立的临床实体,但对于确立诊断的标准尚无共识。本报告的目的是完善诊断LDGL所需的参数。我们研究了从我们机构在三个不同地理区域(北美、欧洲和亚洲)观察的195例病例中挑选出的11例慢性颗粒淋巴细胞增多症患者。这些病例不符合目前纳入LDGL的标准,因为所有患者的颗粒淋巴细胞(GL)均少于2000/微升。然而,在这些患者中的每一例中,我们都发现了离散的GL群体扩增的证据。在所有9例CD3 + LDGL患者的外周血单个核细胞(PBMC)中发现了T细胞受体(TCR)β基因的克隆重排。使用最近产生的针对TCR Vβ基因区域的单克隆抗体(MoAb),我们在研究的3例患者中的每一例的GL上鉴定出一种独特的TCR Vβ。在2例CD3 - LDGL患者中,通过用针对正常自然杀伤(NK)细胞上发现的p58抗原的MoAb染色,我们也鉴定出一种受限的反应模式。这11例GL绝对数量相对较低的患者的临床特征与先前报道的GL大于2000/微升的患者相似。这些数据表明,诸如针对Vβ基因区域和p58分子的MoAb以及分子分析等新技术有助于识别离散的GL增殖的扩增。即使在GL计数相对较低的患者中,受限的GL亚群扩增的证明也是LDGL诊断的证据。我们的结果也有助于在广泛的GL淋巴细胞增多症中区分正常的终点和病理的起点。