Cutting Edge: NKG2D Signaling Enhances NK Cell Responses but Alone Is Insufficient To Drive Expansion during Mouse Cytomegalovirus Infection.
Cutting Edge: NKG2D Signaling Enhances NK Cell Responses but Alone Is Insufficient To Drive Expansion during Mouse Cytomegalovirus Infection.
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尖端：NKG2D信号传导增强了NK细胞反应，但仅在小鼠巨细胞病毒感染过程中，单独使用不足以驱动膨胀。
DOI：
10.4049/jimmunol.1700799
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发表时间：
2017-09-01
期刊：
影响因子：
--
通讯作者：
Lanier LL
中科院分区：
文献类型：
--
作者：
Nabekura T;Gotthardt D;Niizuma K;Trsan T;Jenus T;Jonjic S;Lanier LL
自然杀伤（NK）细胞在宿主防御病毒中起关键作用。在这里，我们研究了小鼠巨细胞病毒（MCMV）感染后NKG 2D在NK细胞扩增中的作用。野生型和NKG 2D缺陷型（Klrk 1-/-）Ly 49 H + NK细胞在感染经过改造以允许表达NKG 2D配体的MCMV毒株时会强劲增殖，从而增强野生型NK细胞的反应。初始NK细胞仅表达NKG 2D-L，仅与DAP 10配对，而活化NK细胞表达的NKG 2D-S与DAP 10或DAP 12配对，类似于Ly 49 H。然而，当小鼠感染这些MCMV毒株时，单独的NKG 2D无法驱动Ly 49 H-NK细胞的稳健扩增，这可能是因为NKG 2D-S在感染后仅瞬时表达。这些结果表明，NKG 2D增强了NK细胞的Ly 49 H依赖性增殖;然而，单独的NKG 2D信号传导不足以扩增NK细胞，这可能是由于NKG 2D-DAP 12复合物仅瞬时表达所致。
Natural killer (NK) cells play a critical role in host defense against viruses. Here, we investigated the role of NKG2D in the expansion of NK cells after mouse cytomegalovirus (MCMV) infection. Wild-type and NKG2D-deficient (Klrk1−/−) Ly49H+ NK cells robustly proliferated when infected with MCMV strains engineered to allow expression of NKG2D ligands, which enhanced the response of wild-type NK cells. Naïve NK cells exclusively express NKG2D-L, which pairs only with DAP10, whereas NKG2D-S expressed by activated NK cells pairs with both DAP10 or DAP12, similar to Ly49H. However, NKG2D alone was unable to drive robust expansion of Ly49H− NK cells when mice were infected with these MCMV strains likely because NKG2D-S was only transiently expressed after infection. These findings demonstrate that NKG2D augments Ly49H-dependent proliferation of NK cells; however, NKG2D signaling alone is inadequate for expansion of NK cells, likely due to only transient expression of a NKG2D-DAP12 complex.
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DOI：
10.1084/jem.20021973
发表时间：
2003-05-19
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Lodoen M;Ogasawara K;Hamerman JA;Arase H;Houchins JP;Mocarski ES;Lanier LL
通讯作者：
Lanier LL
影响因子：
8.7
作者：
Lanier LL
通讯作者：
Lanier LL
DOI：
10.4049/jimmunol.181.9.6394
发表时间：
2008-11-01
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Fodil-Cornu N;Lee SH;Belanger S;Makrigiannis AP;Biron CA;Buller RM;Vidal SM
通讯作者：
Vidal SM
影响因子：
32.4
作者：
Nabekura, Tsukasa;Kanaya, Minoru;Shibuya, Akira;Fu, Guo;Gascoigne, Nicholas R. J.;Lanier, Lewis L.
通讯作者：
Lanier, Lewis L.
影响因子：
32.4
作者：
Bakker, ABH;Hoek, RM;Lanier, LL
通讯作者：
Lanier, LL