敗血症の樹状細胞：病理学的変化と治療的意味

敗血症は、近年、重病患者の主な死因です。樹状細胞（DC）は重要な抗原提示細胞であり、生来および適応免疫を調節することにより免疫応答に重要な役割を果たします。DCの数、DCSへの単球の分化、およびDCの機能に関連する表面分子のレベルは、敗血症の発生において変化します。アポトーシスの誘導、反応性酸素種の生成、WNTシグナル伝達経路の活性化、エピジェネティックな調節、およびToll様受容体依存性シグナル伝達の変動など、敗血症中のDCの変化に関与する多くのメカニズムがあります。このレビューでは、敗血症のDCの変化に関与するDCサブセットとメカニズムの分類を提示し、敗血症のDCを対象とした治療戦略をさらに議論し、異常な免疫応答を改善し、敗血症の進行中に生命を延ばします。

Sepsis is the leading cause of death for critically ill patients in recent years. Dendritic cells (DCs) are important antigen-presenting cells and play a key role in immune response by regulating the innate and adaptive immunity. The number of DCs, the differentiation of monocytes into DCs, and the levels of surface molecules associated with the function of DCs are changed in the development of sepsis. There are many mechanisms involved in the alterations of DCs during sepsis, including the induction of apoptosis, reactive oxygen species generation, activation of the Wnt signaling pathway, epigenetic regulation, and variation in Toll-like receptor-dependent signaling. In this review, we present the classifications of DC subsets and mechanisms involved in the alterations of DCs in sepsis, as well as further discuss the therapeutic strategies targeting DCs in sepsis to improve the aberrant immune response and prolong the life during sepsis progression.