IL-33 Modulates Cytotoxic NK Cell Subsets in Severe Eosinophilic Asthma

Natural Killer (NK) cells contribute to airway inflammation in severe eosinophilic asthma (SEA). IL-33, elevated in SEA, may modulate NK cell function, but its effects are unclear. We analyzed peripheral blood NK cell subsets from five SEA patients and five healthy controls using flow cytometry, assessing CD56/CD16-defined subsets and markers, CD57, NKG2A, CD62L, and ICAM-1, at baseline and after 72 h IL-33 stimulation. SEA patients showed reduced mature cytotoxic NK cells and altered expression of adhesion and regulatory molecules. IL-33 selectively increased ICAM-1 and NKG2A in mature NK cells, while decreasing these markers in immature subsets. These findings indicate that IL-33 differentially regulates NK-cell phenotype and function, highlighting NK cells as dynamic mediators of inflammation in SEA.

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Publication Details

Journal
Life
Published
2026-02-18
DOI
https://doi.org/10.3390/life16020348
Primary Topic
IL-33, ST2, and ILC Pathways
Type
article
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article

IL-33 Modulates Cytotoxic NK Cell Subsets in Severe Eosinophilic Asthma

Laura Bergantini, E Bargagli, Irene Paggi, Paolo CAMELI et al.
Life
IL-33, ST2, and ILC Pathways
article

IL-33 Modulates Cytotoxic NK Cell Subsets in Severe Eosinophilic Asthma

Laura Bergantini, E Bargagli, Irene Paggi, Paolo CAMELI, Tommaso Pianigiani
article en

Abstract

Natural Killer (NK) cells contribute to airway inflammation in severe eosinophilic asthma (SEA). IL-33, elevated in SEA, may modulate NK cell function, but its effects are unclear. We analyzed peripheral blood NK cell subsets from five SEA patients and five healthy controls using flow cytometry, assessing CD56/CD16-defined subsets and markers, CD57, NKG2A, CD62L, and ICAM-1, at baseline and after 72 h IL-33 stimulation. SEA patients showed reduced mature cytotoxic NK cells and altered expression of adhesion and regulatory molecules. IL-33 selectively increased ICAM-1 and NKG2A in mature NK cells, while decreasing these markers in immature subsets. These findings indicate that IL-33 differentially regulates NK-cell phenotype and function, highlighting NK cells as dynamic mediators of inflammation in SEA.

LifeVol. 16(2)
Azienda Ospedaliera Universitaria Senese (IT)
Life below water
Openalex Percentile: Top 50%
IL-33, ST2, and ILC Pathways
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