Toll and Toll-like receptor signalling in development
نویسندگان
چکیده
منابع مشابه
Toll-like receptor 2 signalling and inflammation.
T oll-like receptors (TLRs) are a family of proteins that are involved in the initial phase of host defence against invading pathogens. TLRs act as primary sensors of microbial products and activate signalling pathways that lead to the induction of immune and inflammatory genes. TLRs belong to a broader family of proteins, which include receptors for the proinflammatory cytokines interleukin (I...
متن کاملRole of adapters in Toll-like receptor signalling.
Toll-like receptors (TLRs) play a critical role in the detection of invading pathogens within the body and the subsequent immune response. Individual TLRs recognize distinct microbial components. The TLRs are a type 1 transmembrane receptor that possess an extracellular leucine-rich repeat domain and cytoplasmic domain homologous with that of the interleukin 1 receptor (IL-1R) family. Upon stim...
متن کاملPrion pathogenesis in the absence of Toll-like receptor signalling.
To reach the brain from peripheral sites, prions must colonize various cell types within the lymphoreticular compartment. However, no prion entry receptors are yet known. Toll-like receptors (TLRs) are pattern-recognition receptors that bind a multitude of pathogens and are therefore candidates as effectors of prion entry. Moreover, injection of unmethylated CpG oligodinucleotides, which stimul...
متن کاملA poxviral homolog of the Pellino protein inhibits Toll and Toll-like receptor signalling.
Toll-like receptor (TLR) signalling pathways constitute an evolutionarily conserved component of the host immune response to pathogenic infection. Here, we describe the ability of a virally encoded form of the Pellino protein to inhibit Tolland TLR-mediated activation of downstream Rel family transcription factors. In addition to inhibiting drosomycin promoter activation by Spätzle in Drosophil...
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ژورنال
عنوان ژورنال: Development
سال: 2018
ISSN: 1477-9129,0950-1991
DOI: 10.1242/dev.156018