Fig 2: Results for rhIFN-α stimulation of neutrophils in pSS patients and healthy controls. A Results MitoSOX measurements of pSS and HC plasma stimulation of healthy neutrophils (n=9). B Representative flow cytometry results for the JC-1 staining in pSS patients and healthy controls with or without rhIFN stimulation (HC\pSS-Unstimulated represented for the freshly isolated neutrophils, pSS\HC-with or without rhIFN represented for the neutrophils stimulated with or without rhIFN). C Representative flow cytometry results of ROS production in pSS and healthy neutrophils with or without rhIFN stimulation (HC\pSS-Unstimulated represented for the freshly isolated neutrophils, pSS\HC-with or without rhIFN represented for the neutrophils stimulated with or without rhIFN, different color represented for the different subjects). D Comparison of JC-1 monomer percentage (mitochondrial damage, n=10), ROS production (n=10), and MPO concentration (n=12) between neutrophils stimulated with or without rhIFN-α. E Immunofluorescence staining of NETs-DNA (DAPI, blue) with or without rhIFN stimulation. F IFN-α receptor inhibitor reduced the mitochondrial damage (MitoSOX) and the production of NETs (SytocGreen and MPO levles). *P-value < 0.05, **P-value < 0.01, ***P-value <0.001)

Fig 3: The correlations of biochemical parameters in the caudate and putamen of patients with diseases and disease progression.(A) PAR concentration in the caudate of PDD vs. disease progression. (B) TREM2 concertation in the putamen of PDD vs. disease progression. (C) TSPO density in the putamen of PDD vs. disease progression. (D) PAR concentration in the caudate of LBDs vs. disease progression. (E) TREM2 concentration in the putamen of LBDs vs. disease progression. (F) 8-oxo-dG level in the putamen of AD vs. disease progression. (G) MPO concentration in the caudate of AD vs. disease progression. *P < 0.05, **P < 0.01. Sample size: PD, n = 10; PDD, n = 8; DLB, n = 10; AD, n = 27. 8-oxo-dG: 8-Oxo-7,8-dihydro-2'-deoxyguanosine; AD: Alzheimer disease; DLB: dementia with Lewy bodies; LBDs: Lewy body diseases; MPO: myeloperoxidase; PD: Parkinson disease; PDD: PD dementia; PAR: poly (ADP-ribose); rs: Spearman’s rank correlation coefficient; TREM2: triggering receptors expressed on myeloid cell 2; TSPO: translocator protein.

Fig 4: Impact of biochemical parameters in the striatum on the AD patient survival.Mantel-Cox curve of patient survival according to high molecular level (above the mean value, blue line) and low molecular level (below the mean value, red line) in the caudate and putamen of AD brains. *P < 0.05, ***P < 0.001. 8-oxo-dG: 8-Oxo-7,8-dihydro-2'-deoxyguanosine; AD: Alzheimer disease; MPO: myeloperoxidase.

Fig 5: Enhanced NETosis markers in pSS patients. A Comparison of the fluorescence intensity (FI) of plasma cf-DNA between pSS patients (n=22) and matched healthy controls (n=16), each point represented the fluorescence intensity results of every subjects. B Comparison of the plasma MPO levels between pSS patients, matched healthy controls, and pSS patients after treatment, each point represented the fluorescence intensity results of every subject. C The correlation between plasma cf-DNA and MPO levels. D Comparison of plasma cf-DNA levels and MPO levels between patients with high IgG (n=10) or normal IgG (n=7) levels. E Comparison of Plasma cf-DNA levels and MPO levels between patients with high activity (n=9) or low activity (n=8), patients’ disease activity was assessed through ESSDAI (High activity, ESSDAI>5; low activity, ESSDAI≤5). F,G Comparison of plasma-stimulated neutrophils from pSS and HC to produce NETosis markers, F the fluorescence intensity of cf-DNA; G MPO production levels. H NETosis markers staining in pSS and HC labial glands (×40, blue for DAPI, red for MPO, green for CitH3). *P-value < 0.05, **P-value < 0.01, ***P-value <0.001)