Lupus & antiphospholipid syndrome
Neutrophil transcriptomics in systemic lupus erythematosus (SLE) reveals intrinsic disease signatures, shared ex vivo adaptation, and transcriptional reset after chimeric antigen receptor (CAR) T-cell therapy
Authors' conclusion
Neutrophils in SLE exhibit intrinsic, disease-specific transcriptomic alterations while sharing ex vivo adaptation dynamics with healthy individuals.
Study context
- Population
- Neutrophils isolated via negative selection from patients with SLE and healthy individuals; one patient with SLE undergoing KYV-101 anti-CD19 CAR T-cell therapy
- Participants
- 7 vs 7
- Comparison
- Neutrophils from patients with SLE vs healthy individuals
- SLEn = 7
- Healthyn = 7reference
- Outcome
- Transcriptomic differences in neutrophils between SLE and healthy individuals
Methodological detailsRNA sequencing, ex vivo stimulation with lipopolysaccharide (LPS), longitudinal single-patient analysis after CAR T-cell therapy
- RNA sequencing
- Ex vivo stimulation with LPS
- Longitudinal single-patient analysis after CAR T-cell therapy
Main finding
As reported in the abstract
Neutrophil transcriptome, SLE vs healthy
- Differentially expressed genes consistently distinguishing SLE from healthy neutrophils
- 258
Further findings
Ex vivo adaptation over 60 minutes
- Shared activation pathways, such as NF-κB and apoptosis, in both groups
Response to LPS stimulation
- Overlapping inflammatory responses; retained functional capacities in SLE neutrophils
Neutrophil transcriptomic profile after KYV-101 anti-CD19 CAR T-cell therapy (a patient with SLE) · 3 months posttreatment
- Profiles realigned with healthy controls
- Longitudinal data from a patient with SLE
Original publication
Neutrophil transcriptomics in SLE reveals intrinsic disease signatures, shared ex vivo adaptation, and transcriptional reset after CAR T-cell therapy. Ann Rheum Dis. Published 18 March 2026. doi:10.
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