Department of Pathology, University of Michigan, Ann Arbor, USA.
Epigenetics. 2011 Mar;6(3):273-83. doi: 10.4161/epi.6.3.14017. Epub 2011 Mar 1.
Studies in humans and animal models indicate that profound immunosuppression is one of the chronic consequences of severe sepsis. This immune dysfunction encompasses deficiencies in activation of cells in both the myeloid and lymphoid cell lineages. As a result, survivors of severe sepsis are at risk of succumbing to infections perpetrated by opportunistic pathogens that are normally controlled by a fully functioning immune system. Recent studies have indicated that epigenetic mechanisms may be one driving force behind this immunosuppression, through suppression of proinflammatory gene production and subsequent immune cell activation, proliferation and effector function. A better understanding of epigenetics and post-septic immunosuppression can improve our diagnostic tools and may be an important potential source of novel molecular targets for new therapies. This review will discuss important pathways of immune cell activation affected by severe sepsis, and highlight pathways of epigenetic regulation that may be involved in post-septic immunosuppression.
研究表明，深度免疫抑制是严重败血症的慢性后果之一。这种免疫功能障碍包括骨髓和淋巴谱系细胞激活的缺陷。因此，严重败血症的幸存者面临着被机会性病原体感染的风险，这些病原体通常被功能正常的免疫系统所控制。最近的研究表明，表观遗传机制可能是导致这种免疫抑制的驱动力之一，它通过抑制促炎基因的产生以及随后的免疫细胞激活、增殖和效应功能。更好地了解表观遗传学和败血症后的免疫抑制可以改善我们的诊断工具，并且可能是新疗法的新型分子靶点的重要潜在来源。这篇综述将讨论受严重败血症影响的免疫细胞激活的重要途径，并强调可能参与败血症后免疫抑制的表观遗传调控途径。
