Ohshima K, Suzumiya J, Kato A, Tashiro K, Kikuchi M
Department of Pathology, School of Medicine, Fukuoka University, Japan.
Int J Cancer. 1997 Aug 7;72(4):592-8. doi: 10.1002/(sici)1097-0215(19970807)72:4<592::aid-ijc7>3.0.co;2-l.
Lymph nodes from the incipient or early neoplastic phase of adult T-cell leukemia/lymphoma (ATLL) histologically resemble Hodgkin's disease. Integrated proviral human T-lymphotrophic virus type I (HTLV-I) has been demonstrated in such lesions. We studied 18 patients with this disease, and about half of the cases developed typical ATLL within 2 or 3 years. In all cases, either mono- or oligoclonal cell populations with proviral HTLV-I DNA were detected by Southern blot analysis and/or inverse polymerase chain reaction (IPCR). In addition, either a mono- or oligoclonal rearrangement of T-cell receptor genes was demonstrated. Giant cells with Reed-Sternberg-like histological features revealed CD15 and CD30 positivity. The background infiltrating lymphocytes represented either no or only minimal nuclear abnormalities with a CD4+ T-cell phenotype. In less than half of all cases, Epstein-Barr virus (EBV) infected the giant cells. A mixed EBV-A and -B type was found in 3, and a multiple genotype of EBV lymphocyte-determined membrane antigen (LYDMA) was found in 6 cases. These results could have been due to the immunodeficient status of the patients. A single-cell PCR of the giant cell, B cell, CD4+ or CD8+ T cells could be performed after cell sorting in 4 cases. HTLV-I infection was frequently found in the CD4+ T cells, but in neither the giant cells nor the B cells. The CD4+ T cells exhibited clonality. The giant cells showed various PCR products of IgH, and also expressed recombination activating genes (RAG). In summary, the giant cells were reactive cells, which resembled the immature B-lineage cells, while HTLV-I infected the CD4+ T cells, which demonstrated clonality. Based on these above findings, we consider CD4+ cells to play an important role in ATLL tumorigenesis.
成人T细胞白血病/淋巴瘤(ATLL)初期或早期肿瘤阶段的淋巴结在组织学上类似于霍奇金病。在这类病变中已证实存在整合的I型人嗜T淋巴细胞病毒(HTLV-I)前病毒。我们研究了18例该疾病患者,约一半病例在2或3年内发展为典型的ATLL。在所有病例中,通过Southern印迹分析和/或反向聚合酶链反应(IPCR)检测到带有前病毒HTLV-I DNA的单克隆或寡克隆细胞群。此外,还证实了T细胞受体基因的单克隆或寡克隆重排。具有里德-斯腾伯格样组织学特征的巨细胞显示CD15和CD30阳性。背景浸润淋巴细胞要么没有核异常,要么仅有轻微核异常,呈CD4 + T细胞表型。在不到一半的病例中,爱泼斯坦-巴尔病毒(EBV)感染了巨细胞。3例中发现EBV-A和-B混合型,6例中发现EBV淋巴细胞决定膜抗原(LYDMA)的多基因型。这些结果可能归因于患者的免疫缺陷状态。4例病例在细胞分选后可对巨细胞、B细胞、CD4 +或CD8 + T细胞进行单细胞PCR。HTLV-I感染在CD4 + T细胞中经常发现,但在巨细胞和B细胞中均未发现。CD4 + T细胞表现出克隆性。巨细胞显示出IgH的各种PCR产物,并且还表达重组激活基因(RAG)。总之,巨细胞是反应性细胞,类似于未成熟的B系细胞,而HTLV-I感染了表现出克隆性的CD4 + T细胞。基于上述发现,我们认为CD4 +细胞在ATLL肿瘤发生中起重要作用。