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Purpose of Review <p>Chronic pruritus (CP) is among the most distressing symptoms and has a complex pathophysiology. This review aims to describe the mediators and mechanisms of neuroimmune crosstalk—a term referring the bidirectional interactions between the nervous and immune systems that underly itch pathogenesis and chronicity.</p> Recent Findings <p>Type 2 cytokines (IL-4, IL-13, IL-31) directly activate pruriceptive neurons, resulting in itch sensation and nerve fiber sensitization via TRPV1/TRPA1, whereas keratinocyte-derived alarmins (TSLP and IL-33) amplify neural activation. Periostin, an emerging downstream mediator, binds integrin αVβ3 on neurons and induces macrophage IL-31 release, representing a link between immune and neural pathways. BNP, another emerging mediator that is co-expressed with IL-31, facilitates itch signaling in the spinal cord and induces keratinocyte production of itch mediators, highlighting its integral role in neuroimmune signaling.</p> Summary <p>CP arises from a complex interplay between the immune system, sensory neurons, and keratinocytes. The success of therapeutic advances targeting cytokines, neuropeptides, and their receptors in recent years have confirmed the importance of understanding these complex underlying networks.</p>

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Cross-Talk between Neurons and Immune Cells in Pruritus: from Mechanisms To Medicines

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月19日

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  • Nicole Khalil,
  • Tomer Kagan,
  • Gil Yosipovitch

摘要

Purpose of Review

Chronic pruritus (CP) is among the most distressing symptoms and has a complex pathophysiology. This review aims to describe the mediators and mechanisms of neuroimmune crosstalk—a term referring the bidirectional interactions between the nervous and immune systems that underly itch pathogenesis and chronicity.

Recent Findings

Type 2 cytokines (IL-4, IL-13, IL-31) directly activate pruriceptive neurons, resulting in itch sensation and nerve fiber sensitization via TRPV1/TRPA1, whereas keratinocyte-derived alarmins (TSLP and IL-33) amplify neural activation. Periostin, an emerging downstream mediator, binds integrin αVβ3 on neurons and induces macrophage IL-31 release, representing a link between immune and neural pathways. BNP, another emerging mediator that is co-expressed with IL-31, facilitates itch signaling in the spinal cord and induces keratinocyte production of itch mediators, highlighting its integral role in neuroimmune signaling.

Summary

CP arises from a complex interplay between the immune system, sensory neurons, and keratinocytes. The success of therapeutic advances targeting cytokines, neuropeptides, and their receptors in recent years have confirmed the importance of understanding these complex underlying networks.