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首页> 美国卫生研究院文献>Journal of Virology >Human Uterine Natural Killer Cells but Not Blood Natural Killer Cells Inhibit Human Immunodeficiency Virus Type 1 Infection by Secretion of CXCL12
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Human Uterine Natural Killer Cells but Not Blood Natural Killer Cells Inhibit Human Immunodeficiency Virus Type 1 Infection by Secretion of CXCL12

机译：人子宫自然杀伤细胞但不包括血液自然杀伤细胞通过分泌CXCL12抑制人免疫缺陷病毒1型感染

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Natural killer (NK) cells derived from the human female reproductive tract (FRT) are phenotypically and functionally distinct from those obtained from peripheral blood. Because the FRT is a primary site of human immunodeficiency virus type 1 (HIV-1) infection in women, we determined whether soluble factors secreted by uterine-derived NK (uNK) cells inhibit HIV-1 infection. Clonal populations of uNK cells were activated with interleukin-12 (IL-12) and IL-15, and conditioned media (CM) from these cultures evaluated for their ability to inhibit infection of cells by HIV-1IIIB, HIV-1NL4.3, and HIV-1HC4 (X4-tropic) or HIV-1BaL (R5-tropic) viruses. We found that soluble factors secreted by activated uNK cells significantly inhibited X4-tropic virus infection of TZM-bl cells, peripheral blood mononuclear cells, and primary human endometrial cells, but not infection by HIV-1BaL. In contrast, CM from peripheral blood NK (bNK) cells did not inhibit HIV-1 infection of cells. Analysis of factors secreted from uNK clones with anti-HIV-1 activity demonstrated significantly higher levels of CXCL12 compared to uNK clones without this activity, and the HIV inhibitory activity was neutralized by antibodies to CXCL12. Collectively, these data demonstrate that human uNK cells release chemokines with anti-HIV-1 activity for X4-tropic strains and this suggest that these chemokines may contribute to the inhibition of X4-tropic strain transmission across mucosal tissues.
机译：源自人类女性生殖道（FRT）的自然杀伤（NK）细胞在表型和功能上与从外周血获得的细胞不同。因为FRT是妇女中人类免疫缺陷病毒1型（HIV-1）感染的主要部位，所以我们确定了子宫源性NK（uNK）细胞分泌的可溶性因子是否抑制HIV-1感染。用白介素12（IL-12）和IL-15激活uNK细胞的克隆群，并评估这些培养物中的条件培养基（CM）抑制其被HIV-1IIIB，HIV-1NL4.3，和HIV-1HC4（X4-tropic）或HIV-1BaL（R5-tropic）病毒。我们发现激活的uNK细胞分泌的可溶性因子显着抑制TZM-bl细胞，外周血单核细胞和原代人子宫内膜细胞的X4嗜性病毒感染，但不感染HIV-1BaL。相反，来自外周血NK（bNK）细胞的CM不能抑制HIV-1细胞感染。对具有抗HIV-1活性的uNK克隆分泌的因子的分析表明，与没有该活性的uNK克隆相比，CXCL12的水平明显更高，并且HIV抑制活性被抗CXCL12的抗体所中和。总体而言，这些数据表明，人uNK细胞释放出对X4嗜性菌株具有抗HIV-1活性的趋化因子，这表明这些趋化因子可能有助于抑制X4嗜性菌株在粘膜组织中的传播。

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