Peripheral T-cell lymphoma with Reed-Sternberg-like cells of B-cell phenotype and genotype associated with Epstein-Barr virus infection
Peripheral T-cell lymphoma with Reed-Sternberg-like cells of B-cell phenotype and genotype associated with Epstein-Barr virus infection
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DOI：
10.1097/00000478-199910000-00008
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发表时间：
1999-10-01
影响因子：
5.6
通讯作者：
Jaffe, ES
中科院分区：
文献类型：
--
作者：
Quintanilla-Martinez, L;Fend, F;Jaffe, ES
我们报告三例淋巴结周围T细胞淋巴瘤（PTCL）与里德-斯滕伯格样（RS样）细胞的B细胞表型和/或基因型。所有病例的组织学分析均显示由大小不等的非典型淋巴样细胞引起的弥漫性淋巴结消失。其中2例具有血管免疫母细胞性T细胞淋巴瘤（AILT）的特征。在所有活检组织中，散在大单核细胞和双核细胞，具有显著的嗜酸性核仁和丰富的细胞质，类似于经典RS细胞和单核细胞变体。3例淋巴瘤细胞均为T细胞系（CD 3+、CD 43+和CD 45 RO+）。所有病例的RS样细胞均为CD 30和CD 15阳性。与肿瘤性T细胞相反，RS样细胞缺乏所有T细胞标志物，并且在两种情况下对CD 20呈阳性。所有病例的RS样细胞均检测到EB病毒潜伏膜蛋白1（LMP 1）和EBER 1（2/2）。肿瘤性T细胞EBV阴性。聚合酶链反应（PCR）分析表明，克隆重排的T细胞受体γ链基因在三个案件。病例1和3中免疫球蛋白重链基因重排的显微切割RS样细胞的PCR分析显示寡克隆模式。PTCL中RS样细胞的存在代表了诊断陷阱，因为在一个病例中，该观察结果导致了霍奇金病（HD）的误诊。EBV感染细胞的寡克隆扩增可能与T细胞淋巴瘤和AILT相关的潜在免疫缺陷有关。这种现象可能为某些T细胞淋巴瘤后出现霍奇金病的病例提供了依据，并提示它们是克隆无关的肿瘤。LMP 1的表达似乎是至关重要的免疫表型，并可能为RS和RS样细胞的形态出现在不同的淋巴系统恶性肿瘤，包括HD，慢性淋巴细胞白血病，PTCL。
We report three cases of nodal peripheral T-cell lymphoma (PTCL) with Reed-Sternberg-like (RS-Like) cells of B-cell pheno- and/or genotype. Histologic analysis in all cases revealed diffuse nodal effacement by atypical lymphoid cells of variable size. Two of the three cases had features of angioimmunoblastic T-cell lymphoma (AILT). Large mononuclear and binucleated cells with prominent eosinophilic nucleoli and abundant cytoplasm resembling classic RS cells and mononuclear variants were scattered throughout all biopsies. The lymphoma cells in the three cases were of T-cell lineage (CD3+, CD43+, and CD45RO+). The RS-like cells from all cases were CD30 and CD15 positive. In contrast to the neoplastic T cells, the RS-like cells lacked all T-cell markers and in two cases were positive for CD20. Epstein-Barr virus (EBV) latent membrane protein 1 (LMP1) and EBER 1 (2/2) were detected in the RS-like cells in all cases. The neoplastic T cells were negative for EBV. Polymerase chain reaction (PCR) analysis demonstrated clonal rearrangements of the T-cell receptor gamma chain gene in the three cases. PCR analysis of microdissected RS-like cells for immunoglobulin heavy chain gene rearrangements in cases 1 and 3 showed an oligoclonal pattern. The presence of RS-like cells in PTCL represents a diagnostic pitfall, because in one case this observation led to a misdiagnosis of Hodgkin's disease (HD), The oligoclonal expansion of EBV-infected cells may be related to underlying immunodeficiency associated with T-cell lymphomas and AILT in particular. This phenomenon may provide the basis for some cases of Hodgkin's disease after T-cell lymphomas and suggests that they are clonally unrelated neoplasms. The expression of LMP1 appears to be crucial for the immunophenotype and probably for the morphology of the RS and RS-like cells appearing in diverse lymphoid malignancies, including HD, chronic lymphocytic leukemia, and PTCL.