What is it about?

Inflammatory or post-surgical pain is caused by the interaction between the nervous and immune systems. We have shown for the first time that dendritic cells, immune sentinels in barrier tissues, control the initiation of this pain response through their secreted cytokines CCL17 and CCL22. These two inflammatory mediators bind to the same receptor, CCR4, that is preferentially expressed on sensory (pain) neurons. Activation of the receptor causes their sensitization; blocking CCR4 activity using pharmacological or genetic tools eliminates the pain hypersensitivity observed.

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Why is it important?

The contribution of dendritic cells to pain was poorly defined, and mechanisms regulating pain are critical to the development of new therapeutic tools. Further study will be necessary to identify other inflammatory mediators secreted by these cells that might further contribute to pain outcomes.

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This page is a summary of: Skin-resident dendritic cells mediate postoperative pain via CCR4 on sensory neurons, Proceedings of the National Academy of Sciences, January 2022, Proceedings of the National Academy of Sciences, DOI: 10.1073/pnas.2118238119.
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