Negative regulatory approaches to the attenuation of Toll-like receptor signaling.
Negative regulatory approaches to the attenuation of Toll-like receptor signaling.
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负调控方法是指控受体信号传导的衰减。
DOI：
10.1038/emm.2013.28
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发表时间：
2013-02-22
影响因子：
12.8
通讯作者：
Choi, Sangdun
中科院分区：
文献类型：
--
作者：
Anwar, Muhammad Ayaz;Basith, Shaherin;Choi, Sangdun
Toll样受体(Toll-like Receptor，TLRs)是先天免疫反应的重要组成部分，负责通过诱导炎性分子清除入侵的微生物。这些受体还参与对有害内源性分子的反应，并在激活先天免疫系统和塑造适应性免疫反应方面发挥关键作用。然而，TLR信号通路必须受到严格的调控，因为过度的TLR刺激可能会破坏促炎和抗炎反应之间的微妙平衡。这种干扰可能会通过自身免疫和炎症性疾病的发展而损害宿主，如类风湿性关节炎和系统性红斑狼疮。一些研究已经研究了TLRs的调节通路，它对于调节促炎反应是必不可少的。这些研究报告了几种单独或联合作用于免疫反应的途径和分子。在这篇综述中，我们综述了TLR信号负性调控的研究进展。此外，本文综述了TLR信号在多个水平上的调控，包括接头复合体失稳、信号蛋白的磷酸化和泛素介导的降解、其他受体的操纵以及转录调控。最后，还简要讨论了合成抑制剂，以强调炎症性疾病治疗中的负面调节方法。
Toll-like receptors (TLRs) are pivotal components of the innate immune response, which is responsible for eradicating invading microorganisms through the induction of inflammatory molecules. These receptors are also involved in responding to harmful endogenous molecules and have crucial roles in the activation of the innate immune system and shaping the adaptive immune response. However, TLR signaling pathways must be tightly regulated because undue TLR stimulation may disrupt the fine balance between pro- and anti-inflammatory responses. Such disruptions may harm the host through the development of autoimmune and inflammatory diseases, such as rheumatoid arthritis and systemic lupus erythematosus. Several studies have investigated the regulatory pathways of TLRs that are essential for modulating proinflammatory responses. These studies reported several pathways and molecules that act individually or in combination to regulate immune responses. In this review, we have summarized recent advancements in the elucidation of the negative regulation of TLR signaling. Moreover, this review covers the modulation of TLR signaling at multiple levels, including adaptor complex destabilization, phosphorylation and ubiquitin-mediated degradation of signal proteins, manipulation of other receptors, and transcriptional regulation. Lastly, synthetic inhibitors have also been briefly discussed to highlight negative regulatory approaches in the treatment of inflammatory diseases.
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影响因子：
3.7
作者：
González-López A;Aguirre A;López-Alonso I;Amado L;Astudillo A;Fernández-García MS;Suárez MF;Batalla-Solís E;Colado E;Albaiceta GM
通讯作者：
Albaiceta GM
DOI：
10.1084/jem.20031237
发表时间：
2004-01-05
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Doyle SE;O'Connell RM;Miranda GA;Vaidya SA;Chow EK;Liu PT;Suzuki S;Suzuki N;Modlin RL;Yeh WC;Lane TF;Cheng G
通讯作者：
Cheng G
影响因子：
20.3
作者：
Bhattacharyya, Sandip;Brown, Diane E.;Muglia, Louis J.
通讯作者：
Muglia, Louis J.
影响因子：
4.8
作者：
Butt, Aisha Qasim;Ahmed, Suaad;Miggin, Sinead M.
通讯作者：
Miggin, Sinead M.
DOI：
10.1073/pnas.0510802103
发表时间：
2006-02-21
影响因子：
11.1
作者：
Davis, CN;Mann, E;Bartfai, T
通讯作者：
Bartfai, T