Intact NKG2D-independent function of NK cells chronically stimulated with the NKG2D ligand Rae-1.

Intact NKG2D-independent function of NK cells chronically stimulated with the NKG2D ligand Rae-1.
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DOI:
10.4049/jimmunol.1000397
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发表时间:
2010-07-01
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
通讯作者:
Lanier LL
Lanier LL
中科院分区:
其他
文献类型:
--
作者:
Champsaur M;Beilke JN;Ogasawara K;Koszinowski UH;Jonjic S;Lanier LL

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人类肿瘤经常表达膜结合或可溶性NK组2,成员D(NKG2D)配体。这导致NKG2D在NK和CD8+ T细胞表面上的慢性结合以及受体的快速内化。尽管人们充分认识到这种现象会损害NKG2D依赖性功能,但缺乏对通过NKG2D长期刺激的细胞中NKG2D非依赖性功能的仔细分析。使用慢性NKG2D配体表达的小鼠模型,我们表明,在病毒感染的背景下,持续暴露于NKG2D配体不会在功能上损害NK细胞和CD8+ T细胞。
Human tumors frequently express membrane-bound or soluble NK group 2, member D (NKG2D) ligands. This results in chronic engagement of NKG2D on the surfaces of NK and CD8+ T cells and rapid internalization of the receptor. Although it is well appreciated that this phenomenon impairs NKG2D-dependent function, careful analysis of NKG2D-independent functions in cells chronically stimulated through NKG2D is lacking. Using a mouse model of chronic NKG2D ligand expression, we show that constant exposure to NKG2D ligands does not functionally impair NK cells and CD8+ T cells in the context of viral infection.
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