Impaired T-cell regulation of B-cell growth in Helicobacter pylori-related gastric low-grade MALT lymphoma
Impaired T-cell regulation of B-cell growth in Helicobacter pylori-related gastric low-grade MALT lymphoma
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DOI：
10.1016/s0016-5085(99)70395-1
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发表时间：
1999-11-01
期刊：
影响因子：
29.4
通讯作者：
Del Prete, G
中科院分区：
文献类型：
--
作者：
D'Elios, MM;Amedei, A;Del Prete, G
背景和目标：幽门螺杆菌相关的低度胃粘膜相关淋巴组织（MALT）淋巴瘤的肿瘤性B细胞对T辅助细胞有反应，对H.幽门螺旋杆菌诱导的T细胞帮助。研究方法：将5例MALT淋巴瘤患者胃粘膜T细胞克隆子代与5 H.幽门螺杆菌感染的慢性胃炎患者。结果：评估T细胞克隆对H.幽门螺杆菌，细胞因子谱，有助于B细胞增殖，以及穿孔素或Fas介导的B细胞生长的细胞毒性调节。MALT淋巴瘤的165个CD 4（+）克隆中有28个和慢性胃炎的178个CD 4（+）克隆中有33个识别H. pylori抗原。细胞因子的产生在2个系列的克隆中是相似的。所有MALT淋巴瘤衍生的克隆剂量依赖性地增加其B细胞的帮助，而慢性胃炎的克隆失去了辅助活性的T-B-细胞比大于1，因为伴随的细胞溶解杀死5个细胞。来自MALT淋巴瘤的T细胞克隆具有降低的穿孔素介导的细胞毒性和差的诱导Fas介导的凋亡的能力。这些缺陷仅限于胃T细胞。结论：H.幽门螺杆菌诱导的T细胞依赖性B细胞活化和B细胞生长的细胞毒性控制缺陷可能与H有关。幽门螺杆菌感染、局部T细胞反应和低度胃MALT淋巴瘤的发生。
Background & Aims: Neoplastic B cells of the Helicobacter pylori-related low-grade gastric mucosa-associated lymphoid tissue (MALT) lymphoma are responsive to T helper cells and sensitive to withdrawal of H. pylori-induced T-cell help. Methods: The clonal progeny of T cells from the gastric mucosa of 5 patients with MALT lymphoma was compared with that of T-cell clones obtained from 5 H. pylori-infected patients with chronic gastritis. Results: T-cell clones were assessed for specificity to H. pylori, cytokine profile, help for B-cell proliferation, and perforin- or Fas-mediated cytotoxic regulation of B-cell growth. Twenty-eight of 165 CD4(+) gastric clones from MALT lymphoma and 33 of 178 CD4(+) clones from chronic gastritis recognized H. pylori antigens. Cytokine production was similar in the 2 series of clones. All MALT lymphoma-derived clones dose-dependently increased their B-cell help, whereas clones from chronic gastritis lost helper activity at T-to-B-cell ratios greater than 1 because of concomitant cytolytic killing of 5 cells. T-cell clones from MALT lymphoma had both reduced perforin-mediated cytotoxicity and poor ability to induce Fas-mediated apoptosis. These defects were limited to gastric T cells. Conclusions: H. pylori-induced T cell-dependent B-cell activation and deficient cytotoxic control of B-cell growth may link H. pylori infection, local T-cell response, and genesis of low-grade gastric MALT lymphoma.