MyD88-deficient Hydra reveal an ancient function of TLR signaling in sensing bacterial colonizers
MyD88-deficient Hydra reveal an ancient function of TLR signaling in sensing bacterial colonizers
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DOI：
10.1073/pnas.1213110109
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发表时间：
2012-11-20
影响因子：
11.1
通讯作者：
Bosch, Thomas C. G.
中科院分区：
文献类型：
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作者：
Franzenburg, Soeren;Fraune, Sebastian;Bosch, Thomas C. G.
Toll样受体（TLR）信号通路是脊椎动物先天免疫系统中最重要的信号通路之一。在无脊椎动物中的研究集中在果蝇和线虫秀丽隐杆线虫上，关于TLR信号传导的进化起源和祖先功能的信息很少。在果蝇中，Toll样受体家族的成员参与胚胎发育和先天免疫。In C.在线虫中，TLR同源物TOL-1的明确免疫功能是有争议的，并且脊椎动物TLR信号传导的中心组分（包括关键衔接蛋白髓样分化初级应答基因88（MyD 88）和转录因子NF-κ B）不存在。在诸如刺胞动物Hydra magnipripiata和Nematostella vectensis的基底后生动物中，存在脊椎动物TLR信号级联的所有组分，但它们在免疫中的作用是未知的。在这里，我们使用的MyD 88功能丧失的方法在水螅证明，细菌的识别是TLR信号的祖先功能，这一过程有助于宿主介导的tenonization由细菌以及防御细菌病原体。
Toll-like receptor (TLR) signaling is one of the most important signaling cascades of the innate immune system of vertebrates. Studies in invertebrates have focused on the fruit fly Drosophila melanogaster and the nematode Caenorhabditis elegans, and there is little information regarding the evolutionary origin and ancestral function of TLR signaling. In Drosophila, members of the Toll-like receptor family are involved in both embryonic development and innate immunity. In C. elegans, a clear immune function of the TLR homolog TOL-1 is controversial and central components of vertebrate TLR signaling including the key adapter protein myeloid differentiation primary response gene 88 (MyD88) and the transcription factor NF-kappa B are not present. In basal metazoans such as the cnidarians Hydra magnipapillata and Nematostella vectensis, all components of the vertebrate TLR signaling cascade are present, but their role in immunity is unknown. Here, we use a MyD88 loss-of-function approach in Hydra to demonstrate that recognition of bacteria is an ancestral function of TLR signaling and that this process contributes to both host-mediated recolonization by commensal bacteria as well as to defense against bacterial pathogens.