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Antisense and siRNA as agonists of Toll-like receptors

A Corrigendum to this article was published on 01 January 2005

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Abstract

About 25 years ago, researchers first demonstrated that a short synthetic oligodeoxynucleotide, referred to as antisense, can inhibit replication of Rous sarcoma virus through hybridization to viral RNA. Since then, several hybridization-based oligonucleotide approaches have been developed to elucidate the functions of genes and their potential as therapeutic agents. Short-interfering (si) RNA is the most recent example. To effectively inhibit gene expression, an antisense or siRNA must be resistant to nucleases, be taken up efficiently by cells, hybridize efficiently with the target mRNA and activate selective degradation of the target mRNA or block its translation without causing undesirable side effects. However, both antisense and siRNA agents have been shown to exert non-target-related biological effects including immune stimulation. Do antisense and siRNA agents work as ligands for Toll-like receptors (TLRs), a family of pathogen-associated, molecular pattern recognition receptors?

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Figure 1: Toll-like receptor pathways and antisense.

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  • 01 January 2005

    Nat. Biotechnol. 22, 1533–1537 (2004) The title should read, “Role of Toll-like receptors in antisense and siRNA.” The last line of paragraph 3, beginning “This article summarizes present evidence....” should be deleted. In Table 1, superscript 'b' in “Sequencea,b, should be deleted, and superscript'a' after 3′ in line 3 of that column should be replaced by superscript b.

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Correspondence to Sudhir Agrawal.

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Agrawal, S., Kandimalla, E. Antisense and siRNA as agonists of Toll-like receptors. Nat Biotechnol 22, 1533–1537 (2004). https://doi.org/10.1038/nbt1042

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