Functional Consequences of Interactions between Human NKR-P1A and Its Ligand LLT1 Expressed on Activated Dendritic Cells and B Cells1
Functional Consequences of Interactions between Human NKR-P1A and Its Ligand LLT1 Expressed on Activated Dendritic Cells and B Cells1
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人 NKR-P1A 与其在活化树突细胞和 B 细胞上表达的配体 LLT1 之间相互作用的功能后果1
DOI：
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发表时间：
2008
影响因子：
4.4
通讯作者：
Lewis L. Lanier
中科院分区：
文献类型：
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作者：
D. Rosen;W. Cao;D. Avery;S. Tangye;Yong‐jun Liu;J. P. Houchins;Lewis L. Lanier;Lewis L. Lanier
凝集素样转录物-1（LLT 1）（也称为破骨细胞抑制凝集素或CLEC 2D）是存在于NK细胞和T细胞上的人NKR-P1 A（CD 161）受体的配体。为了进一步了解这种相互作用的生理相关性，我们开发了针对LLT 1的mAb，表征了LLT 1的表达模式，并探索了LLT 1与NK细胞和T细胞上的NKR-P1 A受体接合的功能后果。LLT 1在TLR激活的浆细胞样树突状细胞、TLR激活的单核细胞衍生的树突状细胞以及通过TLR 9、表面IG或CD 40刺激的B细胞上表达。NK细胞上的NKR-P1 A与靶细胞上的LLT 1之间的相互作用抑制NK细胞介导的细胞毒性和细胞因子产生，并可抑制TCR活化的NKR-P1 A + CD 8 + T细胞产生TNF-α。相反，NKR-P1 A不能抑制或增强携带NKR-P1 A的CD 4 + T细胞的TCR依赖性活化。LLT 1在活化的树突状细胞和B细胞上的表达表明它可能调节NK细胞和APC之间的相互作用。
Lectin-like transcript-1 (LLT1) (also named osteoclast inhibitory lectin or CLEC2D) is a ligand for the human NKR-P1A (CD161) receptor, present on NK cells and T cells. To further understand the physiological relevance of this interaction, we developed mAbs against LLT1, characterized the expression pattern of LLT1, and explored the functional consequence of LLT1 engagement of the NKR-P1A receptor on NK cells and T cells. LLT1 is expressed on TLR-activated plasmacytoid dendritic, TLR-activated monocyte-derived dendritic cells, and on B cells stimulated through TLR9, surface Ig, or CD40. Interactions between NKR-P1A on NK cells and LLT1 on target cells inhibit NK cell-mediated cytotoxicity and cytokine production and can inhibit TNF-α production by TCR-activated NKR-P1A+ CD8+ T cells. In contrast, NKR-P1A failed to inhibit or augment the TCR-dependent activation of NKR-P1A-bearing CD4+ T cells. Expression of LLT1 on activated dendritic cells and B cells suggests that it might regulate the cross-talk between NK cells and APCs.
影响因子：
4.2
作者：
Kinsella, TM;Nolan, GP
通讯作者：
Nolan, GP
影响因子：
30.5
作者：
Welte, Stefan;Kuttruff, Sabrina;Steinle, Alexander
通讯作者：
Steinle, Alexander
影响因子：
20.3
作者：
Hanabuchi, S;Watanabe, N;Liu, YJ
通讯作者：
Liu, YJ