Cutting edge:: All-trans retinoic acid down-regulates TLR2 expression and function
Cutting edge:: All-trans retinoic acid down-regulates TLR2 expression and function
复制标题
DOI：
10.4049/jimmunol.174.5.2467
复制
发表时间：
2005-03-01
影响因子：
4.4
通讯作者：
Modlin, RL
中科院分区：
文献类型：
--
作者：
Liu, PT;Krutzik, SR;Modlin, RL
微生物感染的一个主要后果是由宿主炎症反应引起的组织损伤。在痤疮中，炎症部分是由于痤疮丙酸杆菌激活TLR2的能力。由于全反式维甲酸（ATRA）可以减少痤疮的炎症，我们研究了它是否调节TLR2的表达和拍卖。用A - TRA处理原代人单核细胞导致TLR2及其辅助受体CD14下调，但TLR1和TRL4不下调。TLR2/1配体触发单核细胞因子释放的能力被ATRA预处理和共处理抑制；然而，TLR4的激活仅受共处理的影响。ATRA还能下调痤疮假单胞细胞因子诱导。这些数据表明，A - TRA通过两种途径对单核细胞发挥抗炎作用，一种途径特异性影响TLR2/1和CD14的表达，另一种途径独立于TLR的表达。靶向TLR表达和功能的药物代表了治疗人类炎症的新策略。
A major consequence of microbial infection is the tissue injury that results from the host inflammatory response. In acne, inflammation is due in part to the ability of Propionibacterium acnes to activate TLR2. Because all-trans retinoic acid (ATRA) decreases inflammation in acne, we investigated whether it regulates TLR2 expression and Auction. Treatment of primary human monocytes with A TRA led to the down-regulation of TLR2 as well as it's coreceptor CD14, but not TLR1 or TRL4. The ability of a TLR2/1 ligand to trigger monocyte cytokine release was inhibited by pre- and cotreatment with ATRA; however, TLR4 activation was affected by cotreatment only. ATRA also down-regulated monocyte cytokine induction by P. acnes. These elata indicate that A TRA exerts an anti-inflammatory effect on monocytes via two pathways, one specifically affecting TLR2/1 and CD14 expression and one independent of TLR expression. Agents that target TLR expression and function represent a novel strategy to treat inflammation in humans.