Interleukin-17A as a Potential Mediator in Inflammatory Mechanisms of Insomnia

May 4, 2026Neurochemical research

Interleukin-17A's Possible Role in Inflammation Linked to Insomnia

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Circadian Biology on OpenScience ↗PubMed ↗DOI ↗

Abstract

Increased IL-17A serum levels may be linked to poor sleep quality.

Insomnia is associated with changes in immune expression, particularly involving cytokines.
Cytokines such as IL-1β, IL-6, and TNF-α have established connections to sleep behavior and circadian rhythms.
Emerging evidence suggests that IL-17A could play a role in sleep disturbances and neuroinflammation.
The specific relationship between IL-17A and insomnia disorder remains largely unexplored.
Previous studies indicate that elevated IL-17A levels may correlate with poor sleep quality in individuals with insomnia and comorbid conditions.

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The interaction between immune cytokines and sleep can be bidirectional, and the circadian rhythm balance has a crucial role to the immune and inflammatory regulation. Insomnia is a prevalent sleep disorder, in which occur modifications in immune expression, including the cytokines pattern. Some somnogenic cytokines, such as interleukin (IL)-1β, IL-6 and tumor necrosis factor-α (TNF-α) have been classically recognized for their direct association with sleep behavior and circadian alignment. More recent evidence has increasingly implicated the role of IL-17A in sleep disturbances and neuroinflammation. However, its specific relationship with insomnia disorder remains underexplored. This cytokine is considered as a relevant immune component in the pathways involved in inflammatory and autoimmune issues. Previous and rare studies on the behavior of IL-17A in insomnia related with comorbid disease suggested that increased IL-17A serum levels may be linked to poor sleep quality. We suggest that further experimental and clinical studies examining the role of IL-17A should shed more light in its relationship with insomnia; and on the immunological and neuroinflammatory associations with this sleep disorder.

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Interleukin-17A as a Potential Mediator in Inflammatory Mechanisms of Insomnia

Abstract

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