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CD161B:ClrB相互作用介导自然杀伤细胞与树突状细胞共培养后肿瘤靶细胞增强裂解的激活。

CD161B:ClrB interactions mediate activation of enhanced lysis of tumor target cells following NK cell:DC co-culture.

作者信息

Yang Tianbing, Flint Melanie S, Webb Katie M, Chambers William H

机构信息

University of Pittsburgh Cancer Institute, University of Pittsburgh, Pittsburgh, PA 15213-1863, USA.

出版信息

Immunol Res. 2006;36(1-3):43-50. doi: 10.1385/IR:36:1:43.

Abstract

Co-culture of natural killer (NK) cells and dendritic cells (DCs) results in their reciprocal co-activation, and an enhancement of lysis of tumor target cells. The receptor:ligand pairings mediating this enhancement are unknown. Therefore, we investigated whether interactions of CD161, on NK cells, with Clrs, on DCs, might have a role in this effect. Blocking expression of CD161B using siRNA resulted in a reduction in enhanced lytic activity following NK:DC co-culture. Conversely, blocking expression of CD161F with siRNA had no effect on enhanced lytic function following NK:DC co-culture. Blocking expression of ClrB/Ocil, a ligand for CD161B, resulted in a reduced level of enhanced lytic function following NK:DC co-culture. This is the first report of NK receptors responsible for interaction with DCs having a role in mediating enhanced lytic function following NK:DC interactions.

摘要

自然杀伤(NK)细胞与树突状细胞(DC)的共培养导致它们相互共激活,并增强对肿瘤靶细胞的裂解作用。介导这种增强作用的受体-配体配对尚不清楚。因此,我们研究了NK细胞上的CD161与DC细胞上的Clr之间的相互作用是否可能在这种效应中发挥作用。使用小干扰RNA(siRNA)阻断CD161B的表达会导致NK:DC共培养后增强的裂解活性降低。相反,用siRNA阻断CD161F的表达对NK:DC共培养后增强的裂解功能没有影响。阻断CD161B的配体ClrB/Ocil的表达会导致NK:DC共培养后增强的裂解功能水平降低。这是关于负责与DC相互作用的NK受体在介导NK:DC相互作用后增强的裂解功能中发挥作用的首次报道。

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