小柯机器人

英国剑桥大学Francesco Colucci研究小组发现，CD94/NKG2A抑制受体可改造子宫NK细胞，从而改善人类和小鼠的妊娠结局。2021年4月21日，《免疫》杂志在线发表了这项成果。

研究人员表示，几乎所有人类细胞和约50％的小鼠子宫自然杀伤（uNK）细胞均表达保守的CD94/NKG2A抑制受体。NKG2A与人HLA-E和小鼠Qa-1结合，可驱动NK细胞改造，这是受HLA-B等位基因影响的过程，其生理重要性仍然未知。

研究人员发现，与野生型雄性交配的母鼠中的NKG2A基因敲除在妊娠中引起未最佳的母亲血管反应，伴有胎盘基因表达紊乱、胎儿体重减轻，且具有不对称生长的较小胎儿比例增加以及大脑发育异常。这些是子痫前期人类综合症的特征。在对7,219个先兆子痫病例的全基因组关联研究中，研究人员发现与不利于NKG2A教育的母亲HLA-B等位基因相关的相对风险增加了7％。

这些结果表明，母亲的HLA-B→HLA-E→NKG2A途径有助于健康怀孕，并可能对子代健康产生影响，从而建立了与NK细胞改造有关的生理学意义。

附：英文原文

Title: The CD94/NKG2A inhibitory receptor educates uterine NK cells to optimize pregnancy outcomes in humans and mice

Author: Norman Shreeve, Delphine Depierreux, Delia Hawkes, James A. Traherne, Ulla Sovio, Oisin Huhn, Jyothi Jayaraman, Amir Horowitz, Hormas Ghadially, John R.B. Perry, Ashley Moffett, John G. Sled, Andrew M. Sharkey, Francesco Colucci

Issue&Volume: 2021-04-21

Abstract: The conserved CD94/NKG2A inhibitory receptor is expressed by nearly all human and～50% of mouse uterine natural killer (uNK) cells. Binding human HLA-E and mouse Qa-1,NKG2A drives NK cell education, a process of unknown physiological importance influencedby HLA-B alleles. Here, we show that NKG2A genetic ablation in dams mated with wild-type malescaused suboptimal maternal vascular responses in pregnancy, accompanied by perturbedplacental gene expression, reduced fetal weight, greater rates of smaller fetuseswith asymmetric growth, and abnormal brain development. These are features of thehuman syndrome pre-eclampsia. In a genome-wide association study of 7,219 pre-eclampsiacases, we found a 7% greater relative risk associated with the maternal HLA-B allele that does not favor NKG2A education. These results show that the maternalHLA-B→HLA-E→NKG2A pathway contributes to healthy pregnancy and may have repercussionson offspring health, thus establishing the physiological relevance for NK cell education.

DOI: 10.1016/j.immuni.2021.03.021

Source: https://www.cell.com/immunity/fulltext/S1074-7613(21)00133-3

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