Myeloid differentiation factor 88-independent Toll-like receptor pathway: Sustaining inflammation or promoting tolerance?
Myeloid differentiation factor 88-independent Toll-like receptor pathway: Sustaining inflammation or promoting tolerance?
复制标题
DOI：
10.1016/j.biocel.2007.04.021
复制
发表时间：
2007-01-01
影响因子：
4
通讯作者：
Tergaonkarl, Vinay
中科院分区：
文献类型：
--
作者：
Biswas, Subhra K.;Tergaonkarl, Vinay
toll样受体信号是宿主先天免疫的主要分子通路。从机制上讲，它可以分为两个不同的级联：髓细胞分化因子88依赖性级联和髓细胞分化因子88非依赖性级联（或Toll受体相关干扰素激活因子介导）级联。髓样分化因子88依赖性信号传导是所有toll样受体共同的，除了toll样受体3，它专门利用髓样分化因子88非依赖性途径。基于最近的证据，本文提出骨髓分化因子88独立通路不仅在革兰氏阴性感染中维持炎症反应，而且在内毒素耐受等保护性反应中可能发挥作用。我们假设骨髓分化因子88独立通路激活的延迟动力学可能在功能上旨在通过促进细胞耐受性来调节炎症反应，并可能保护宿主免受炎症诱导的损伤。未来的研究需要通过实验验证这一观点，以及骨髓分化因子88独立通路的重要相关性。(c) 2007 Elsevier Ltd.版权所有。
Toll-like receptor signaling represents a principal molecular pathway for host innate immunity. Mechanistically, it can be segregated into two distinct cascades: the myeloid differentiation factor 88-dependent and myeloid differentiation factor 88-independent (or Toll receptor-associated activator of interferon-mediated) cascades. Myeloid differentiation factor 88-dependent signaling is common to all the Toll-like receptors, except Toll-like receptor 3, which exclusively utilizes the myeloid differentiation factor 88-independent pathway. Based on recent evidences, a possible role for myeloid differentiation factor 88-independent pathway not only in sustaining inflammatory responses during Gram-negative infection but also in protective responses like endotoxin tolerance is proposed in this review. We hypothesize that the delayed kinetics of activation of the myeloid differentiation factor 88-independent pathway might be functionally aimed at tuning-down inflammatory reactions through promotion of cellular tolerization and possibly protecting hosts from inflammation-induced injury. Future studies will be needed to experimentally validate this idea and the crucial relevance of the myeloid differentiation factor 88-independent pathway. (c) 2007 Elsevier Ltd. All rights reserved.