Antitumor response of regional lymph node lymphocytes in human lung cancer
Antitumor response of regional lymph node lymphocytes in human lung cancer
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DOI：
10.1007/s002620050523
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发表时间：
1998-12-01
影响因子：
5.8
通讯作者：
Nomoto, K
中科院分区：
文献类型：
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作者：
Takenoyama, M;Yasumoto, K;Nomoto, K
我们最近报道，区域淋巴结淋巴细胞（RLNL）从原发性肺癌患者处于更高的激活状态比外周血淋巴细胞（PBL）时，活化相关分子的FAGS分析研究。为探讨RLNL对自体肿瘤细胞（AT）的反应能力，本文应用混合淋巴细胞肿瘤细胞反应（MLTR）对41例原发性肺癌进行了研究。在41例无IL-2的患者中，20例（48.8%）和41例有IL-2的患者中，23例（56.1%）发现对AT的显著增殖反应。另一方面，在30例无IL-2的病例中的8例（26.7%）和30例有IL-2的病例中的11例（36.7%）的PBL中观察到这种应答。MLTR与旋切器大小等临床因素无明显相关性。为了进一步分析RLNL的抗AT反应，研究了AT刺激后RLNL的细胞因子产生。在MLTR阳性反应的RLNL中观察到干扰素-γ（IFN-γ）产生的增加，而在PBL中未发现这种增加。最后，为了阐明MHC II类分子的表达是否是MLTR的关键点，通过免疫组织化学染色检测原发性病变中的肿瘤细胞中MHC II类分子的表达，并使用抗MHC II类单克隆抗体进行MLTR的阻断试验。结果表明，肿瘤组织中MHC Ⅱ类分子的表达与MLTR呈正相关，抗MHC Ⅱ类分子单克隆抗体可部分阻断MLTR。这些结果表明，RLNL对AT比PBL处于更高的活化状态，这一发现被认为有助于提高我们对RLNL在肺癌患者中的作用的理解。
We recently reported that regional lymph node lymphocytes (RLNL) from patients with primary lung cancer were in a more highly activated state than peripheral blood lymphocytes (PBL) when the activation-related molecules were studied by FAGS analysis. To identify whether or not RLNL had the ability to respond to autologous tumor cells (AT), in the present study a mixed lymphocyte tumor cell reaction (MLTR) either with or without recombinant interleukin 2 (rIL-2) was performed in 41 cases with primary lung cancer. Significant proliferative responses to AT were found in RLNL from 20 of 41 cases (48.8%) without IL-2, and in 23 of 41 cases (56.1%) with IL-2. On the other hand, such responses were observed in the PBL from 8 of 30 cases (26.7%) without IL-2, and from 11 of 30 cases (36.7%) with IL-2. No significant correlation between MLTR and such clinical factors as turner size. metastasis to lymph node, histology and stage of the disease was found. To further analyze the anti-AT response of RLNL, the cytokine production of RLNL was investigated after stimulation by AT. An increase in interferon-gamma (IFN-gamma) production was observed in RLNL with a positive reaction of MLTR, while no such increase was found in PBL. Finally, to elucidate whether the expression of MHC class II molecules was a key point in MLTR, tumor cells in primary lesions were examined for the expression of MHC class II by immunohistochemical staining, and the blocking assay of MLTR was performed with anti-MHC class II monoclonal antibody. Data suggested that there was a positive correlation between MHC class II expression of the tumor and MLTR and that MLTR were partially blocked by anti-MHC class II monoclonal antibody. These results demonstrated that RLNL were in a more highly activated state against AT than were PBL, and this finding is considered to be helpful in enhancing our understanding of the role of RLNL in lung cancer patients.