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肿瘤性B细胞上抑制性受体ILT3的表达与慢性淋巴细胞白血病的淋巴组织受累有关。

Expression of inhibitory receptor ILT3 on neoplastic B cells is associated with lymphoid tissue involvement in chronic lymphocytic leukemia.

作者信息

Colovai Adriana I, Tsao Lawrence, Wang Su, Lin Hana, Wang Chuan, Seki Tetsunori, Fisher Julie G, Menes Manuel, Bhagat Govind, Alobeid Bachir, Suciu-Foca Nicole

机构信息

Department of Pathology, Columbia University, New York, NY 10032, USA.

出版信息

Cytometry B Clin Cytom. 2007 Sep;72(5):354-62. doi: 10.1002/cyto.b.20164.

Abstract

T cell responses against leukemia-associated antigens have been reported in chronic lymphocytic leukemia (CLL). However, the relentless accumulation of CLL B cells in some patients indicates that anti-tumor immune responses are inefficient. Inhibitory receptors from the Ig-like transcript (ILT) family, such as ILT3 and ILT4, are crucial to the tolerogenic activity of antigen presenting cells. In this study, we examined the expression of ILT3 on CD5+ B cells obtained from 47 patients with CLL. Using flow cytometry and RT-PCR, we found that B CLL cells from 23 of 47 patients expressed ILT3 protein and mature ILT3 mRNA. ILT3 protein and mRNA were not found in normal B cells obtained from donors without CLL. Expression of ILT4 in normal and B CLL cells showed a pattern similar to ILT3. The frequency of ILT3 positive CLL B cells was higher in patients with lymphoid tissue involvement, suggesting that ILT3 may have prognostic value in CLL. Our findings indicate that expression of ILT3 and ILT4 on CLL B cells represents a phenotypic abnormality that may play a role in tolerization of tumor-specific T cells.

摘要

在慢性淋巴细胞白血病(CLL)中已报道了针对白血病相关抗原的T细胞反应。然而,一些患者中CLL B细胞的持续积累表明抗肿瘤免疫反应效率低下。来自免疫球蛋白样转录物(ILT)家族的抑制性受体,如ILT3和ILT4,对抗抗原呈递细胞的致耐受性活性至关重要。在本研究中,我们检测了47例CLL患者的CD5 + B细胞上ILT3的表达。使用流式细胞术和逆转录聚合酶链反应(RT-PCR),我们发现47例患者中有23例的B CLL细胞表达ILT3蛋白和成熟的ILT3 mRNA。在无CLL供体获得的正常B细胞中未发现ILT3蛋白和mRNA。正常和B CLL细胞中ILT4的表达显示出与ILT3相似的模式。在有淋巴组织受累的患者中,ILT3阳性CLL B细胞的频率更高,这表明ILT3可能在CLL中具有预后价值。我们的研究结果表明,CLL B细胞上ILT3和ILT4的表达代表了一种表型异常,可能在肿瘤特异性T细胞的耐受中起作用。

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