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首页> 外文期刊>Immunology: An Official Journal of the British Society for Immunology >Distinct contribution of protein kinase C delta and protein kinase C epsilon in the lifespan and immune response of human blood monocyte subpopulations
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Distinct contribution of protein kinase C delta and protein kinase C epsilon in the lifespan and immune response of human blood monocyte subpopulations

机译：蛋白激酶Cδ和蛋白激酶Cε在人类血液单核细胞亚群的寿命和免疫应答中的不同贡献

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Monocytes, key components of the immune system, are a heterogeneous population comprised of classical monocytes (CD16(-)) and non-classical monocytes (CD16(+)). Monocytes are short lived and undergo spontaneous apoptosis, unless stimulated. Dysregulation of monocyte numbers contribute to the pathophysiology of inflammatory diseases, yet the contribution of each subset remains poorly characterized. Protein kinase C (PKC) family members are central to monocyte biology; however, their role in regulating lifespan and immune function of CD16(-) and CD16(+) monocytes has not been studied. Here, we evaluated the contribution of PKC and PKC epsilon in the lifespan and immune response of both monocyte subsets. We showed that CD16(+) monocytes are more susceptible to spontaneous apoptosis because of the increased caspase-3, -8 and -9 activities accompanied by higher kinase activity of PKC. Silencing of PKC reduced apoptosis in both CD16(+) and CD16(-) monocytes. CD16(+) monocytes express significantly higher levels of PKC epsilon and produce more tumour necrosis factor- in CD16(+) compared with CD16(-) monocytes. Silencing of PKC epsilon affected the survival and tumour necrosis factor- production. These findings demonstrate a complex network with similar topography, yet unique regulatory characteristics controlling lifespan and immune response in each monocyte subset, helping define subset-specific coordination programmes controlling monocyte function.
机译：单核细胞是免疫系统的关键组成部分，是由经典单核细胞（CD16（-））和非经典单核细胞（CD16（+））组成的异质群体。单核细胞寿命短，除非受到刺激，否则会自发凋亡。单核细胞数目的失调促成炎性疾病的病理生理学，但是每个亚组的贡献仍然缺乏特征。蛋白激酶C（PKC）家族成员对单核细胞生物学至关重要。但是，尚未研究它们在调节CD16（-）和CD16（+）单核细胞的寿命和免疫功能中的作用。在这里，我们评估了PKC和PKCε在两个单核细胞亚群的寿命和免疫应答中的贡献。我们显示CD16（+）单核细胞更易于自发凋亡，因为caspase-3，-8和-9活性增加，同时PKC的激酶活性更高。沉默PKC减少CD16（+）和CD16（-）单核细胞的凋亡。与CD16（-）单核细胞相比，CD16（+）单核细胞表达明显更高水平的PKCε，并在CD16（+）中产生更多的肿瘤坏死因子-。 PKCε沉默会影响存活率和肿瘤坏死因子的产生。这些发现证明了一个复杂的网络，具有相似的地形，但是具有独特的调节特性，可控制每个单核细胞亚群的寿命和免疫应答，从而有助于定义控制单核细胞功能的亚群特异性协调程序。

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