Protein kinase networks that limit TLR signalling
Protein kinase networks that limit TLR signalling
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DOI：
10.1042/bst20130124
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发表时间：
2014-02-01
影响因子：
3.9
通讯作者：
Clark, Kristopher
中科院分区：
文献类型：
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作者：
Clark, Kristopher
TLRs(Toll样受体)检测入侵的微生物，从而触发对抗感染所需的促炎介质的产生。虽然这些信号网络是保护宿主免受病原体入侵所必需的，但TLR通路的失调导致了慢性炎症性疾病和自身免疫性疾病的发展。因此，分子机制已经进化到限制TLR信号的强度。在目前的综述中，我重点介绍了我们对蛋白激酶网络的理解的最新进展，该网络通过负向调节TLR信号和/或促进抗炎细胞因子的分泌来抑制先天免疫反应。我介绍了我在IKK(核因子kappa B激酶抑制物)相关的激酶和SIKS(盐诱导的激酶)在该领域更广泛的背景下限制先天免疫方面的关键作用的发现。
TLRs (Toll-like receptors) detect invading micro-organisms which triggers the production of pro-inflammatory mediators needed to combat infection. Although these signalling networks are required to protect the host against invading pathogens, dysregulation of TLR pathways contributes to the development of chronic inflammatory diseases and autoimmune disorders. Molecular mechanisms have therefore evolved to restrict the strength of TLR signalling. In the present review, I highlight recent advances in our understanding of the protein kinase networks required to suppress the innate immune response by negatively regulating TLR signalling and/or promoting the secretion of anti-inflammatory cytokines. I present my discoveries on the key roles of the IKK (inhibitor of nuclear factor kappa B kinase)-related kinases and the SIKs (salt-inducible kinases) in limiting innate immunity within the greater context of the field.