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树突状细胞(dendritic cell,DC)是机体内主要的抗原提呈细胞,可通过其相关受体,如Toll样受体(Toll-like receptor,TLR)感知外界病原微生物的刺激,从而激活下游免疫反应。由于共栖菌及宿主自身表达的TLR配体亦可激活炎性反应信号通路,因此宿主细胞,如DC有可能在静息稳态接触此类活化性配体,基于此,论文作者推测在静息稳态下,细胞内亦有某些蛋白参与控制DC的活化及免疫稳态的维持。A20是一种经典的免疫负向调控蛋白,可通过去泛素化及E3泛素连接酶功能参与调控转录因子NF-κB的活化。A20缺陷(A20-/-)小鼠自发产生严重的炎症疾病,并于围产期致死。
Dendritic cells (DCs) are the major antigen-presenting cells in the body and can be activated downstream by their cognate receptors such as Toll-like receptors (TLRs) immune response. As co-bacteria and host self-expressed TLR ligands can also activate the inflammatory response signaling pathway, host cells, such as DCs, may be exposed to such activating ligands in resting homeostasis. Based on this, the authors speculate that resting Steady state, there are also some proteins in the cell involved in the control of DC activation and immune homeostasis maintenance. A20 is a classical immune negative regulatory protein that can regulate the activation of transcription factor NF-κB through de-ubiquitination and E3 ubiquitin ligase function. A20-deficient (A20 - / -) mice spontaneously developed severe inflammatory disease and died during the perinatal period.