Autoinflammatory & rare systemic diseases
Distinct Natural Killer Cell Signature in Still Disease: Insights From a Multinational Immunome Project Consortium for Autoinflammatory Disorders
Authors' conclusion
Our findings establish NK cell apoptosis, exhaustion, and cytokine unresponsiveness as defining immunologic features of Still disease, distinguishing it from other inflammatory diseases in this cohort.
Study context
- Population
- International cohort of patients with distinct systemic autoinflammatory diseases and healthy controls121 patients + 32 healthy controls
- Participants
- 53 / 23 / 23 / 22 / 32
- Comparison
- Natural killer (NK) cell phenotype in Still disease vs other systemic autoinflammatory diseases and healthy controls
- Still diseasen = 53
- Chronic recurrent multifocal osteomyelitisn = 23
- FMFn = 23
- Inflammation of unknown originn = 22
- Healthy controlsn = 32reference
- Outcome
- Comprehensive NK cell phenotyping
Methodological detailsmultinational cohort, Immunome Project Consortium for Autoinflammatory Disorders
- Multinational cohort
- Immunome Project Consortium for Autoinflammatory Disorders
Main finding
As reported in the abstract
NK cell signature in Still disease
- Reduced NK cell frequency and elevated Fas expression in Still disease, with greater susceptibility to in vitro Fas ligand-induced apoptosis
- Fas ligand expressed by Still disease monocytes and CD38+HLA-DR+ cycling lymphocytes
- Still disease NK cells hyperactivated but exhausted, incl. cytokine unresponsiveness; not observed in the other groups
- NK cell dysfunctional profile normalised during clinical remission
- Exposure of healthy NK cells to IL-12, IL-15 and IL-18 recapitulates the Still disease-associated phenotype
- Transcriptomic profiling identified miR-146a as a potential regulator of NK cell dysfunction
Original publication
Distinct Natural Killer Cell Signature in Still Disease: Insights From a Multinational Immunome Project Consortium for Autoinflammatory Disorders. Arthritis Rheumatol. Published 22 February 2026. doi:10.
Composed by AI from the published abstract and checked against it. How Briefs are made →