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Functional consequences of CD36 downregulation by TLR signals

机译：TLR信号使CD36下调的功能后果

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TLR recognition activates the secretion of pro- and anti-inflammatory cytokines and it also modulates the expression of crucial molecules involved in phagocytosis and antimicrobial activity. Scavenger receptors can act as TLR co-receptors or facilitate antigen loading. However, it remains unknown whether TLR can modulate the expression of these scavenger receptors. We stimulated human peripheral blood mononuclear cells (PBMC) with TLR2 (Pam3CSK4 and FSL1) and TLR4 ligand lipopolysaccharide (LPS) and then analyzed CD36 expression on different monocyte subpopulations by flow cytometry. TLR2 and TLR4 ligands can downregulate CD36 on the surface of monocytes, guiding the protein to intracellular compartments. Even though TLR-activation induced TNFα, IL-10 and IL-6 production, only recombinant TNFα was able to downregulate CD36. Neutralizing anti-TNFα antibodies showed that the Pam3CSK4 and FSL1-induced downregulation was partially mediated by TNFα but not by IL-6 or IL-10. However, LPS-induced downregulation could have also been caused by direct TLR4 targeting and signaling, and/or mediated by other unknown factors. CD36 downregulation reduced the capability of monocytes to phagocyte apoptotic neutrophils. In conclusion, modulation of scavenger receptor expression by TLR targeting on monocytes has functional consequences. Characterization this complex regulation may help us to understand this innate response and develop specific therapeutic drugs for each mechanism.
机译：TLR识别可激活促炎和抗炎细胞因子的分泌，还可以调节参与吞噬作用和抗菌活性的关键分子的表达。清道夫受体可以充当TLR共受体或促进抗原加载。但是，TLR是否可以调节这些清道夫受体的表达仍然未知。我们用TLR2（Pam3CSK4和FSL1）和TLR4配体脂多糖（LPS）刺激了人类外周血单核细胞（PBMC），然后通过流式细胞术分析了CD36在不同单核细胞亚群上的表达。 TLR2和TLR4配体可以下调单核细胞表面的CD36，从而将蛋白质引导至细胞内区室。即使TLR激活诱导了TNFα，IL-10和IL-6的产生，也只有重组TNFα能够下调CD36。中和性抗TNFα抗体显示Pam3CSK4和FSL1诱导的下调部分由TNFα介导，而不是由IL-6或IL-10介导。但是，LPS诱导的下调也可能由直接TLR4靶向和信号传导引起，和/或由其他未知因素介导。 CD36的下调降低了单核细胞吞噬细胞凋亡中性粒细胞的能力。总之，TLR靶向单核细胞对清道夫受体表达的调节具有功能性后果。表征这种复杂的调控机制可能有助于我们理解这种先天的反应，并为每种机制开发特定的治疗药物。

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