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Toll-like receptor 7 mediates pruritus

Nature Neuroscience volume 13, pages 1460–1462 (2010)Cite this article

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Abstract

Toll-like receptors are typically expressed in immune cells to regulate innate immunity. We found that functional Toll-like receptor 7 (TLR7) was expressed in C-fiber primary sensory neurons and was important for inducing itch (pruritus), but was not necessary for eliciting mechanical, thermal, inflammatory and neuropathic pain in mice. Our results indicate that TLR7 mediates itching and is a potential therapeutic target for anti-itch treatment in skin disease conditions.

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Figure 1: Intact pain, but impaired itch, in Tlr7−/− mice.
Figure 2: Scratches induced by imiquimod.
Figure 3: Expression of functional TLR7 in DRG neurons.

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Acknowledgements

The work was supported by US National Institutes of Health grants R01-DE17794, R01-NS54362 and R01-NS67686 to R.-R.J.

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Author notes

  1. Tong Liu, Zhen-Zhong Xu and Chul-Kyu Park: These authors contributed equally to this work.

Authors and Affiliations

  1. Department of Anesthesiology, Sensory Plasticity Laboratory, Pain Research Center, Perioperative and Pain Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA

    Tong Liu, Zhen-Zhong Xu, Chul-Kyu Park, Temugin Berta & Ru-Rong Ji

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  1. Tong Liu
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  2. Zhen-Zhong Xu
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  3. Chul-Kyu Park
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  4. Temugin Berta
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Contributions

T.L. conducted behavioral tests for itch and acute pain and participated in experimental design and manuscript preparation. Z.-Z.X. performed immunohistochemistry and behavioral tests of pain. C.-K.P. conducted single-cell PCR and electrophysiology. T.B. performed in situ hybridization. R.-R.J. supervised the project, designed experiments and wrote the manuscript.

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Correspondence to Ru-Rong Ji.

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The authors declare no competing financial interests.

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Supplementary Figures 1–10 and Supplementary Methods (PDF 1330 kb)

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Liu, T., Xu, ZZ., Park, CK. et al. Toll-like receptor 7 mediates pruritus. Nat Neurosci 13, 1460–1462 (2010). https://doi.org/10.1038/nn.2683

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