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首页> 外文期刊>Cancer letters >Epstein-Barr virus-positive pyothorax-associated lymphoma expresses CCL17 and CCL22 chemokines that attract CCR4-expressing regulatory T cells
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Epstein-Barr virus-positive pyothorax-associated lymphoma expresses CCL17 and CCL22 chemokines that attract CCR4-expressing regulatory T cells

机译：Epstein-BARR病毒阳性斑纹淋巴瘤表达CCL17和CCL22趋化因子，吸引CCR4表达的调节性T细胞

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摘要

Epstein-Barr virus (EBV)-positive diffuse large B-cell lymphomas associated with chronic inflammation (DLBCL-CI) develop in patients with chronic inflammation but without any predisposing immunodeficiency. Given the expression of the EBV latent genes, DLBCL-CI should have mechanisms for evasion of host antitumor immunity. EBV-positive pyothorax-associated lymphoma (PAL) is a prototype of DLBCL-CI and may provide a valuable model for the study of immune evasion by DLBCL-CI. This study demonstrates that PAL cell lines express and secrete CCL17 and/or CCL22 chemokines, the ligands of C-C motif chemokine receptor 4 (CCR4), in contrast to EBV-negative DLBCL cell lines. Accordingly, culture supernatants of PAL cell lines efficiently attracted CCR4-positive regulatory T (Treg) cells in human peripheral blood mononuclear cells. PAL cells injected into mice also attracted CCR4-expressing Treg cells. Furthermore, this study confirmed that CCR4-expressing Treg cells were abundantly present in primary PAL tissues. Collectively, these findings provide new insight into the mechanisms of immune evasion by PAL, and further studies are warranted on whether such mechanisms eventually lead to the development of DLBCL-CI.
机译：对慢性炎症患者的慢性炎症（DLBCL-CI）的慢性炎症（DLBCL-CI）相关，但没有任何易受免疫缺陷的慢性炎症（DLBCL-CI）相关的氨膨胀大B细胞淋巴瘤。鉴于EBV潜基因的表达，DLBCL-CI应具有厌恶宿主抗扰度的机制。 EBV阳性素瘤相关的淋巴瘤（PAL）是DLBCL-CI的原型，可以为DLBCL-CI进行免疫逃逸的研究。该研究表明，与EBV阴性DLBCL细胞系相比，PAL细胞系快递和分泌CCL17和/或CCL22趋化因子，C-C基质趋化因子受体4（CCR4）的配体。因此，PAL细胞系的培养上清液有效地吸引了人外周血单核细胞中的CCR4阳性调节性T（Treg）细胞。注射到小鼠中的PAL细胞也吸引了CCR4表达的Treg细胞。此外，该研究证实，表达CCR4的Treg细胞在原发性PL组织中大量存在。总的来说，这些调查结果为PAL的免疫逃避机制提供了新的洞察力，并有权对这些机制是否最终导致DLBCL-CI的发展进行了进一步的研究。

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