Cellular and molecular characterisation of the peripheral immune environment in migraine
Abstract. Introduction:. Peripheral immune dysfunction may be critically involved in the pathophysiology of migraine. Some evidence supports a role for peripheral T cells, monocytes, and humoral factors including kynurenine metabolites and cytokines, however a comprehensive picture has yet to emerge...
Saved in:
| Main Authors: | , , , , , , , , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Wolters Kluwer
2025-10-01
|
| Series: | PAIN Reports |
| Online Access: | http://journals.lww.com/painrpts/fulltext/10.1097/PR9.0000000000001317 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| Summary: | Abstract. Introduction:. Peripheral immune dysfunction may be critically involved in the pathophysiology of migraine. Some evidence supports a role for peripheral T cells, monocytes, and humoral factors including kynurenine metabolites and cytokines, however a comprehensive picture has yet to emerge.
Objective:. This study sought to undertake a systematic assessment of the immune changes in episodic and chronic migraine across phases of the migraine cycle.
Methods:. Migraine patients in different phases of the migraine cycle with a confirmed diagnosis of episodic or chronic migraine and age- and sex-matched healthy controls were recruited. Peripheral blood was assessed for circulating immune cells, plasma proteins, and kynurenine pathway metabolites in a cross-sectional case–control design. Data were acquired using high-dimensional approaches including proteomics, single-cell mass cytometry, and imaging flow cytometry.
Results:. Plasma proteins related to increased cell–cell adhesion and altered enzymatic activity were increased in migraine. The migraine prodrome displayed a strong and distinct proinflammatory phenotype defined by increased platelet-neutrophil aggregation, quinolinic acid production, and matrix metalloproteinase-9 expression. Migraine patients in the attack phase instead expressed higher levels of cytokine receptors and phosphorylated transcription factors in Th17 cells, monocytes, natural killer cells, and B cells. T cells were shifted to a mobilised, recirculating phenotype across all migraine phases. Episodic and chronic migraine patients were only distinguished by subtle changes in T-cell phenotype.
Conclusion:. Distinct proinflammatory peripheral signatures were detected between migraine phases, while few alterations distinguished episodic and chronic status. These data provide a resource that may aid in the identification of peripheral immune cells and mediators contributing to migraine attack onset. |
|---|---|
| ISSN: | 2471-2531 |