当前位置: X-MOL 学术Allergol. Immunopathol. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Echinococcus multilocularis induces surface high expression of inhibitory killer immunoglobulin-like receptor on natural killer cells.
Allergologia et Immunopathologia ( IF 1.8 ) Pub Date : 2021-09-01 , DOI: 10.15586/aei.v49i5.465
Bayindala X 1 , He Huang 1 , Song Gao 1 , Xinjian Xu 2
Affiliation  

Alveolar echinococcosis (AE) is a malignant and fatal parasitic disease caused by the larvae of Echinococcus multilocularis (E. multilocularis), which inhibits the activity and proliferation of natural killer (NK) cells. In this study, the functional alteration of hepatic NK cells and their related molecules were studied. The AE-infected patient's tissue was fixed with formalin, embedded in paraffin, and stained with Masson's trichrome or hematoxylin and eosin (H&E). Single cells from AE-infected patient or E. multilocularis-infected mice were blocked with Fc-receptor (FcR), and stained with monoclonal antibodies, including CD16, CD56, CD3, KIR2DL1, granzyme B, perforin, Interferon gamma (IFN-γ), and tumor necrosis factor-α (TNFα) or isotype control, to measure molecules and cytokines of NK cells and analyzed by flow cytometry. The Sirius red staining was used to quantitate hepatic fibrosis by calculating quantitative collagen deposition. AE can adjust both the number of hepatic CD56+ NK cells and its KIR2DL1 expression processes. Moreover, the overexpression of KIR2DL1 in NK cells could downregulate the functioning of immune cells in the liver area close to parasitic lesions. The number and dysfunction of NK cells in E. multilocularis infection could be related to the molecule dynamics of cell surface inhibitory receptor Ly49A, leading to hepatic damage and progression of fibrosis. This study illustrated significant increase in hepatic fibrogenesis and apparent upregulation of hepatic CD56+ NK cell population and its KIR2DL1 expression in AE-infected patients. This opposite variation might be related to the impaired NK cells functioning, such as granzyme B, IFN-γ, and TNF-α secretion. In addition, the cell surface inhibitory receptor Ly49A was related to the intracellular cytokine secretion functions of NK cells.

中文翻译:

Echinococcus multilocularis 诱导自然杀伤细胞表面抑制性杀伤免疫球蛋白样受体的高表达。

泡型棘球蚴病(AE)是由多房棘球绦虫(E. multilocularis)的幼虫引起的一种恶性致命的寄生虫病,它抑制自然杀伤(NK)细胞的活性和增殖。在这项研究中,研究了肝NK细胞及其相关分子的功能改变。AE 感染患者的组织用福尔马林固定,石蜡包埋,并用马森三色或苏木精和伊红 (H&E) 染色。来自 AE 感染患者或 E. multilocularis 感染小鼠的单细胞用 Fc 受体 (FcR) 阻断,并用单克隆抗体染色,包括 CD16、CD56、CD3、KIR2DL1、颗粒酶 B、穿孔素、干扰素 γ (IFN-γ ) 和肿瘤坏死因子-α (TNFα) 或同种型对照,以测量 NK 细胞的分子和细胞因子并通过流式细胞术进行分析。天狼星红染色用于通过计算定量胶原沉积来定量肝纤维化。AE 可以调节肝脏 CD56+ NK 细胞的数量及其 KIR2DL1 表达过程。此外,NK细胞中KIR2DL1的过表达可以下调靠近寄生虫病灶的肝脏区域免疫细胞的功能。E. multilocularis 感染中 NK 细胞的数量和功能障碍可能与细胞表面抑制性受体 Ly49A 的分子动力学有关,导致肝损伤和纤维化进展。该研究表明 AE 感染患者的肝纤维化显着增加和肝 CD56+ NK 细胞群及其 KIR2DL1 表达的明显上调。这种相反的变化可能与受损的 NK 细胞功能有关,例如颗粒酶 B、IFN-γ、和 TNF-α 的分泌。此外,细胞表面抑制受体Ly49A与NK细胞的细胞内细胞因子分泌功能有关。
更新日期:2021-09-01
down
wechat
bug