Szondy Zsuzsa, Sarang Zsolt, Kiss Beáta, Garabuczi Éva, Köröskényi Krisztina
Department of Biochemistry and Molecular Biology of Medical Faculty, University of Debrecen, Debrecen, Hungary.
Department of Basic Medical Sciences of Dental Faculty, University of Debrecen, Debrecen, Hungary.
Front Immunol. 2017 Aug 2;8:909. doi: 10.3389/fimmu.2017.00909. eCollection 2017.
In the human body, billions of cells die by apoptosis every day. The subsequent clearance of apoptotic cells by phagocytosis is normally efficient enough to prevent secondary necrosis and the consequent release of cell contents that would induce inflammation and trigger autoimmunity. In addition, apoptotic cells generally induce an anti-inflammatory response, thus removal of apoptotic cells is usually immunologically silent. Since the first discovery that uptake of apoptotic cells leads to transforming growth factor (TGF)-β and interleukin (IL)-10 release by engulfing macrophages, numerous anti-inflammatory mechanisms triggered by apoptotic cells have been discovered, including release of anti-inflammatory molecules from the apoptotic cells, triggering immediate anti-inflammatory signaling pathways by apoptotic cell surface molecules phagocyte receptors, activating phagocyte nuclear receptors following uptake and inducing the production of anti-inflammatory soluble mediators by phagocytes that may act paracrine or autocrine mechanisms to amplify and preserve the anti-inflammatory state. Here, we summarize our present knowledge about how these anti-inflammatory mechanisms operate during the clearance of apoptotic cells.
在人体中，每天有数十亿细胞通过凋亡死亡。随后通过吞噬作用对凋亡细胞的清除通常足够有效，以防止继发性坏死以及随之而来的细胞内容物释放，这些细胞内容物会引发炎症并触发自身免疫。此外，凋亡细胞通常会诱导抗炎反应，因此凋亡细胞的清除通常在免疫上是不活跃的。自从首次发现吞噬凋亡细胞会导致吞噬巨噬细胞释放转化生长因子（TGF）-β和白细胞介素（IL）-10以来，已经发现了许多由凋亡细胞触发的抗炎机制，包括凋亡细胞释放抗炎分子、凋亡细胞表面分子通过吞噬细胞受体触发即时抗炎信号通路、吞噬后激活吞噬细胞核受体以及诱导吞噬细胞产生抗炎可溶性介质，这些介质可能通过旁分泌或自分泌机制发挥作用，以放大和维持抗炎状态。在这里，我们总结了我们目前关于这些抗炎机制在凋亡细胞清除过程中如何运作的知识。
