Simian Immunodeficiency Virus Infection Induces Expansion of α4β7+ and Cytotoxic CD56+ NK Cells
Simian Immunodeficiency Virus Infection Induces Expansion of α4β7+ and Cytotoxic CD56+ NK Cells
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DOI：
10.1128/jvi.01126-10
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发表时间：
2010-09-01
影响因子：
5.4
通讯作者：
Johnson, R. Paul
中科院分区：
文献类型：
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作者：
Reeves, R. Keith;Evans, Tristan I.;Johnson, R. Paul
在此，我们证明，慢性猿猴免疫缺陷病毒（SIV）感染诱导猕猴NK细胞上肠道归巢标记α 4 β 7的显著上调，以及淋巴结运输标记CCR 7的下调。有趣的是，在幼稚动物中，α 4 β 7表达与NK细胞活化增加相关，并且在CD 16（+）NK细胞上，描绘了独特的双功能细胞毒性-CD 107 a（+）/γ干扰素（IFN-γ）分泌群体。然而，虽然SIV感染增加了刺激的CD 56（+）NK细胞上的CD 107 a表达，但α 4 β 7（+）和α 4 β 7（-）NK细胞受到类似的影响。这些发现表明SIV感染将NK细胞从淋巴结重定向到肠道粘膜，但改变了NK细胞功能，而与运输库无关。
Herein we demonstrate that chronic simian immunodeficiency virus (SIV) infection induces significant upregulation of the gut-homing marker alpha 4 beta 7 on macaque NK cells, coupled with downregulation of the lymph node-trafficking marker, CCR7. Interestingly, in naive animals, alpha 4 beta 7 expression was associated with increased NK cell activation and, on CD16(+) NK cells, delineated a unique dual-function cytotoxic-CD107a(+)/gamma interferon (IFN-gamma)-secreting population. However, while SIV infection increased CD107a expression on stimulated CD56(+) NK cells, alpha 4 beta 7(+) and alpha 4 beta 7(-) NK cells were affected similarly. These findings suggest that SIV infection redirects NK cells away from the lymph nodes to the gut mucosae but alters NK cell function independent of trafficking repertoires.