Calreticulin Release at an Early Stage of Death Modulates the Clearance by Macrophages of Apoptotic Cells.

摘要: Calreticulin (CRT) is a well-known "eat-me" signal harbored by dying cells participating in their recognition phagocytes. CRT also recognized to deeply impact the immune response altered self-cells. In this study, we focus on role of newly exposed following cell death induction. We show that if increases at outer face plasma membrane and well C1q even when phosphatidylserine not yet detected, released surrounding milieu able interact with observed exogenous endocytosed THP1 macrophages through macropinocytosis internalization associated particular phenotype characterized an increase spreading migration, upregulation CD14, interleukin-8 release, decrease early apoptotic uptake. Importantly, CRT-induced pro-inflammatory was confirmed human monocytes-derived overexpression CD40 CD274, found monocyte-derived display peculiar polarization notably downregulation histocompatibility complex class II molecules hampering its description classical M1/M2 dichotomy. Altogether our results highlight soluble strong possible consequences macrophage-mediated cell.