Changes in activatory and inhibitory natural killer (NK) receptors may induce progression to multiple myeloma: Implications for tumor evasion of T and NK cells
Changes in activatory and inhibitory natural killer (NK) receptors may induce progression to multiple myeloma: Implications for tumor evasion of T and NK cells
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DOI：
10.1016/j.humimm.2009.07.004
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发表时间：
2009-10-01
期刊：
影响因子：
2.7
通讯作者：
Ruiz-Cabello, Francisco
中科院分区：
文献类型：
--
作者：
Bernal, Monica;Garrido, Pilar;Ruiz-Cabello, Francisco
意义不明的单克隆丙种球蛋白病（MGUS）进展为恶性单克隆丙种球蛋白病的分子基础仍然知之甚少。最近有人提出，这一过程涉及先天性和适应性免疫的抑制。在这项研究中，我们研究了无丙种球蛋白病（对照）和MGUS、多发性骨髓瘤（MM）和浆细胞白血病患者骨髓浆细胞的免疫原性差异。我们检测到主要组织相容性复合体（MHC）I类表达、MHC I类链相关分子A和CD 95的差异，这些差异在MGUS和MM样本之间更为明显：在从MGUS到MM的转变过程中，自然杀伤（NK）细胞激活和抑制信号之间似乎存在严重的不平衡。我们的结果表明，人类白细胞抗原（HLA）I类-亮，云母（暗/-），在骨髓瘤细胞中报告的CD 95（dim/-）免疫表型可能是恶性细胞与细胞毒性T细胞和NK细胞广泛相互作用的结果，似乎是为了逃避免疫监视而进行的免疫编辑。(C)2009年美国组织相容性和免疫遗传学学会。爱思唯尔公司出版All rights reserved.
The molecular basis of monoclonal gammopathy of undetermined significance (MGUS) progression to a malignant monoclonal gammopathy remains poorly understood. It was recently suggested that this process involves the suppression of innate and adaptive immunity. In this study, we examined immunogenic differences in bone marrow plasma cells among individuals without gammopathy (controls) and patients with MGUS, multiple myeloma (MM), and plasma cell leukemia. We detected differences in major histocompatibility complex (MHC) class I expression, MHC class I chain-related molecule A, and CD95 that were more evident between MGUS and MM samples: there appeared to be a critical imbalance between natural killer (NK)-cell activating and inhibitory signals during the transition from MGUS to MM. Our results indicate that the human leukocyte antigen (HLA) class I-bright, MICA(dim/-), and CD95(dim/-) immunophenotype reported in myeloma cells may result from an extensive interaction of malignant cells with cytotoxic T and NK cells and appears to be immunoedited for the evasion of immunosurveillance. (C) 2009 American Society for Histocompatibility and Immunogenetics. Published by Elsevier Inc. All rights reserved.