Hsu S M, Xie S S, Waldron J A
Department of Pathology, University of Arkansas for Medical Sciences, Little Rock.
Am J Pathol. 1992 Oct;141(4):915-23.
A possible autocrine effect of interleukin-6 (IL-6) on the growth and differentiation of the tumor cells of 55 B-cell lymphomas was examined. Interleukin-6 was detected in a few types of B-cell lymphomas, including polymorphic immunocytoma (PI), small lymphocytic lymphoma (SLL), and immunoblastic lymphoma (IBL) with or without plasmacytoid differentiation. In PI and in IBL with plasmacytoid differentiation (IBL-P), IL-6 was detected only in immunoglobulin-containing plasmacytoid cells, and it was absent from most proliferating (Ki-67/PCNA-positive) lymphoma cells. In SLL, IL-6 was not observed in lymphoplasmacytoid cells; instead, IL-6 was observed in transformed (Ki-67/PCNA-positive) tumor cells in proliferation centers. The lymphoplasmacytoid cells in SLL exhibited a phenotype (IL-6/glutathione-S-transferase-pi [GST-pi]-negative), different from that of normal plasma cells (IL-6-negative/GST-pi-positive) and from the plasmacytoid cells (IL-6/GST-pi-positive) in PI and IBL-P. In IBL without obvious plasmacytoid differentiation, IL-6 was detected in most tumor cells that were highly proliferative (Ki-67/PCNA-positive). In this study, IL-6 was undetectable in most lymphomas related to follicular centers, in lymphoblastic lymphoma, in small noncleaved cell lymphomas of the Burkitt and non-Burkitt types, and in diffuse large cell lymphoma. This finding is compatible with a previous finding that IL-6 mRNA was absent from follicular center cells in reactive lymphoid tissues. The functions of IL-6 in these lymphomas may be quite diverse. It appears that IL-6, as an autocrine factor, is responsible for the plasmacytoid differentiation of lymphoma cells in IP and some IBL (IBL-P). The differentiation of lymphoplasmacytoid lymphoma cells in SLL, however, may not be mediated by an autocrine IL-6 mechanism. Interleukin-6 may provide a growth signal, rather than acting as a differentiation factor, for some IBL cells and for some transformed tumor cells in proliferation centers in SLL.
研究了白细胞介素-6（IL-6）对55例B细胞淋巴瘤肿瘤细胞生长和分化的可能自分泌作用。在几种类型的B细胞淋巴瘤中检测到了白细胞介素-6，包括多形性免疫细胞瘤（PI）、小淋巴细胞淋巴瘤（SLL）以及有或无浆细胞样分化的免疫母细胞淋巴瘤（IBL）。在PI和有浆细胞样分化的IBL（IBL-P）中，仅在含免疫球蛋白的浆细胞样细胞中检测到IL-6，而大多数增殖的（Ki-67/PCNA阳性）淋巴瘤细胞中未检测到。在SLL中，淋巴浆细胞样细胞中未观察到IL-6；相反，在增殖中心的转化（Ki-67/PCNA阳性）肿瘤细胞中观察到了IL-6。SLL中的淋巴浆细胞样细胞表现出一种表型（IL-6/谷胱甘肽-S-转移酶-pi [GST-pi]阴性），不同于正常浆细胞（IL-6阴性/GST-pi阳性）以及PI和IBL-P中的浆细胞样细胞（IL-6/GST-pi阳性）。在无明显浆细胞样分化的IBL中，在大多数高增殖（Ki-67/PCNA阳性）的肿瘤细胞中检测到了IL-6。在本研究中，在大多数与滤泡中心相关的淋巴瘤、淋巴母细胞淋巴瘤、伯基特和非伯基特类型的小无裂细胞淋巴瘤以及弥漫性大细胞淋巴瘤中未检测到IL-6。这一发现与先前在反应性淋巴组织的滤泡中心细胞中未检测到IL-6 mRNA的发现一致。IL-6在这些淋巴瘤中的功能可能相当多样。似乎IL-6作为一种自分泌因子，负责IP和一些IBL（IBL-P）中淋巴瘤细胞的浆细胞样分化。然而，SLL中淋巴浆细胞样淋巴瘤细胞的分化可能不是由自分泌IL-6机制介导的。白细胞介素-6可能为一些IBL细胞以及SLL增殖中心的一些转化肿瘤细胞提供生长信号，而不是作为分化因子发挥作用。
