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首页> 外文期刊>Modern Pathology >Differential Expression of Thymus and Activation Regulated Chemokine and Its Receptor CCR4 in Nodal and Cutaneous Anaplastic Large-Cell Lymphomas and Hodgkin's Disease
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Differential Expression of Thymus and Activation Regulated Chemokine and Its Receptor CCR4 in Nodal and Cutaneous Anaplastic Large-Cell Lymphomas and Hodgkin's Disease

机译：胸腺和皮肤间变性再生性大细胞淋巴瘤和霍奇金病中胸腺的差异表达和活化调节的趋化因子及其受体CCR4

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Recent studies demonstrated that Hodgkin/Reed-Sternberg (H/RS) cells in Hodgkin's disease (HD) express thymus and activation-regulated chemokine (TARC), whereas reactive lymphocytes surrounding H/RS cells express its ligand, CC-chemokine receptor 4 (CCR4). Because in vitro studies showed that CCR4 expression is a marker for lymphocytes bearing a T-helper 2 (Th2) phenotype, it was suggested that expression of TARC is a new immune escape mechanism in HD. To find out whether this mechanism might also be operative in CD30+ malignant lymphomas other than HD, TARC and CCR4 expression was investigated by immunohistochemistry on paraffin and frozen-tissue sections of 39 nodal CD30+ anaplastic large cell lymphomas (ALCL), including 27 ALK-negative and 12 ALK-positive ALCL, 25 primary cutaneous CD30+ ALCL, including 11 patients with lymphomatoid papulosis, and 31 cases of HD. TARC was expressed by the neoplastic cells in 12/27 (44%) nodal ALK-negative ALCL and all cases of classic HD, but not in nodal ALK-positive ALCL (0/12) and only rarely in primary cutaneous CD30+ ALCL (3/25). In contrast, CCR4 was expressed by the neoplastic cells in 9/9 cutaneous CD30+ ALCL, and in 9/15 (60%) nodal ALK-negative ALCL, but only in 1/4 (25%) nodal ALK-positive ALCL and not by the H/RS cells in HD (0/8). Apart from three cases of HD showing 10 to 15% CCR4-positive lymphocytes surrounding TARC-positive H/RS cells, CCR4-positive reactive T cells were few (<5%) in all other cases studied. Our results demonstrate a differential expression of TARC and CCR4 in different types of CD30+ malignant lymphomas. The small number of CCR4-positive reactive T cells in most cases studied argues against an important role of TARC expression in the evasion of antitumor responses.
机译：最近的研究表明，霍奇金病（HD）中的霍奇金/里德-斯特恩伯格（H / RS）细胞表达胸腺和激活调节趋化因子（TARC），而H / RS细胞周围的反应性淋巴细胞表达其配体CC趋化因子受体4（ CCR4）。因为体外研究表明CCR4表达是带有T-helper 2（Th2）表型的淋巴细胞的标志物，所以表明TARC的表达是HD的一种新的免疫逃逸机制。为了找出这种机制是否还可以用于除HD以外的CD30 +恶性淋巴瘤，通过免疫组织化学方法对39例CD30 +间变性大细胞淋巴瘤（ALCL）（包括27例ALK阴性）的石蜡和冷冻组织切片进行了免疫组织化学研究，研究了TARC和CCR4的表达。 12例ALK阳性ALCL，25例原发性皮肤CD30 + ALCL，包括11例淋巴瘤样丘疹病和31例HD。 TARC在12/27（44％）淋巴结ALK阴性ALCL和所有经典HD病例中均由肿瘤细胞表达，但在淋巴结ALK阳性ALCL（0/12）中不表达，在原发性皮肤CD30 + ALCL中很少表达（ 3/25）。相比之下，CCR4在9/9皮肤CD30 + ALCL和9/15（60％）淋巴结ALK阴性ALCL中表达，但在1/4（25％）淋巴结ALK阳性ALCL中表达。而不是HD（0/8）中的H / RS单元。除了3例HD病例显示TARC阳性H / RS细胞周围有10％至15％的CCR4阳性淋巴细胞外，在所有其他研究病例中，CCR4阳性反应性T细胞很少（<5％）。我们的结果表明，在不同类型的CD30 +恶性淋巴瘤中TARC和CCR4的差异表达。在大多数研究中，少数CCR4阳性反应性T细胞反对TARC表达在逃避抗肿瘤反应中的重要作用。

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