Editorial Highlights TLR-3 Receptors

Upon recognition, TLR-3 induces the activation of NF-kB (nuclear factor kappa-light-chain-enhancer of activated B cells) to increase production of type I interferons, which signal other cells to increase their antiviral defenses.

TLR-3 receptors are located in the endoplasm of the cells most likely to be exposed and infected by dsRNA (double-stranded RNA) viruses. These include epithelial cells, a broad range of antigen-processing cells, tissue dendritic cells, monocytes, mast cells, NK cells, and others. TLR-3 signaling results in a local cytokine burst that is cell-specific in character and results in a local inflammatory response adaptively selected to provide the greatest chance of infection control for the tissue in question.

The editorial, which was published in the March 15, 2010, edition of the journal Immunotherapy, highlighted recent advances in the fundamental understanding of the toll like receptor pathways, notably TLR-3 and their potential as pharmaceutical targets. In particular, the authors discussed the potential use of the experimental drug Ampligen, manufactured by Hemispherx Biopharma (Philadelphia, PA, USA). This drug, a commercial formulation of the compound polyIC12U, has been advanced to late-stage clinical development as therapy for chronic fatigue syndrome. Chronic fatigue syndrome has been associated with chronic retroviral infection, suggesting that the clinical activity of Apligen may be related to antiviral properties.

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