The mechanisms by which circulating macrophages and their liver counterparts (Kupffer and hepatic stellate cells) alter CD8+ T-cell activity

巨噬细胞等先天免疫细胞协调T细胞的反应是适应性免疫的一个标志。巨噬细胞亚群的细胞因子的产生和细胞与细胞的接触对CD4+T细胞亚群分化的影响已经得到了很好的描述，但它们对CD8+T细胞活性和细胞溶解(CTL)功能的控制尚不清楚。血源性巨噬细胞最近被描述为M1、M2a、2b和2c亚群，建立炎症、免疫调节或组织修复细胞因子环境。此外，组织特异性巨噬细胞在维持免疫耐受、平衡CD8+T细胞渗入的免疫反应和组织破坏效应方面的作用仍有待充分描述。例如，在非酒精性脂肪性肝病中，肝脏驻留巨噬细胞(Kupffer细胞，KC和肝星状细胞，HSC)最近被描述极化为M1和M2样表型，但它们对M2a，2b或2c亚群分化的可能性尚未被研究。M1和M2亚群固有的促炎和抗炎特性可能增强或抑制CD8+T细胞活性和CTL功能。

The orchestration of T-cell responses by innate immune cells such as macrophages is a hallmark of adaptive immunity. The effect of cytokine production and cell-cell contact of macrophage subsets has been well described for CD4+ T-cell subset differentiation, while their control of CD8+ T-cell activity and cytolytic (CTL) function remains unclear. Blood-derived macrophages have been recently described to polarize into M1, M2a, 2b and 2c subsets, establishing inflammatory, immunoregulatory or tissue-repairing cytokine milieus. In addition, the role of tissue-specific macrophages in maintaining immune tolerance and balancing the immune response and tissue destructive effects of infiltrating CD8+ T-cells remains to be fully described. For example, liver resident macrophages (Kupffer cells, KC, and hepatic stellate cells, HSC) have recently been described to polarize to M1- and M2-like phenotypes in non-alcoholic fatty liver disease, yet their potential for M2a, 2b or 2c subset differentiation has not been investigated. The inherent pro- and anti-inflammatory attributes of M1 and M2 subsets may enhance or inhibit CD8+ T-cell activity and CTL function.