A heterogeneous mixture of lipids called oxPAPC, derived from dying cells, can hyperactivate dendritic cells (DCs) but not macrophages. Hyperactive DCs are defined by their ability to release interleukin-1 (IL-1) while maintaining cell viability, endowing these cells with potent aptitude to stimulate adaptive immunity. Herein, we found that the bacterial lipopolysaccharide receptor CD14 captured extracellular oxPAPC and delivered these lipids into the cell to promote inflammasome-dependent DC hyperactivation. Notably, we identified two specific components within the oxPAPC mixture that hyperactivated macrophages, allowing these cells to release IL-1 for several days, by a CD14-dependent process. In murine models of sepsis, conditions that promoted cell hyperactivation resulted in inflammation but not lethality. Thus, multiple phagocytes are capable of hyperactivation in response to oxPAPC, with CD14 acting as the earliest regulator in this process, serving to capture and transport these lipids to promote inflammatory cell fate decisions.

来自死亡细胞的脂质异质混合物oxPAPC可以使树突状细胞（DC）过度活化，但不能使巨噬细胞活化。机能亢进的DCs通过释放白介素-1（IL-1）的能力来维持细胞活力，赋予这些细胞强大的能力以刺激适应性免疫，从而定义了它们。在这里，我们发现细菌脂多糖受体CD14捕获细胞外oxPAPC，并将这些脂质传递到细胞中，以促进炎症小体依赖性DC超活化。值得注意的是，我们在oxPAPC混合物中发现了两个特定的成分，这些成分使巨噬细胞过度活化，从而使这些细胞通过CD14依赖性过程释放IL-1数天。在脓毒症的鼠模型中，促进细胞过度活化的条件导致炎症但没有致死性。因此，