(A) Phospho-H2AX levels are significantly increased in CD4+ T cells, CD8+ T cells and monocytes from SLE compared with those from healthy controls (p=2.16×10−4,

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Figure 2 Shared genetic loci in systemic autoimmune diseases
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Time between systemic lupus erythematosus (SLE) and haematological malignancy diagnoses. Time between systemic lupus erythematosus (SLE) and haematological.
IRF4 is required for anabolic induction of CD4+ T cells.
Time course for laboratory parameters of a patient with systemic lupus erythematosus prior and during bortezomib therapy (arrow). Time course for laboratory.
Main fields of interest.
Fig. 2 TLR8 is aberrantly expressed on pDCs from SSc patients.
Fig. 1 pDCs infiltrate the skin of SSc patients and spontaneously secrete IFN-α and CXCL4. pDCs infiltrate the skin of SSc patients and spontaneously secrete.
Correlation between disease activity and phospho-H2AX levels at G0/G1, S and G2 cell-cycle phases in primary CD3+ T cells and monocytes from patients with.
Mean Safety of Estrogens in Lupus Erythematosus National Assessment–Systemic Lupus Erythematosus Disease Activity Index (SELENA-SLEDAI) score at the last.
Lupus Foundation of America-Rapid Evaluation of Activity in Lupus (LFA-REAL) comprised seven anchored Visual Analogue Scales (0–100 mm each) and can describe.
TLR9 deficiency promotes aberrant T cell and myeloid dendritic cell (DC) phenotype in imiquimod-induced autoimmunity. TLR9 deficiency promotes aberrant.
Vaccination induces activation of cTFH cells and transient ASCs
Association of B cell TLR4 levels to disease activity.
2/A Comparison of IP-10 and SIGLEC1 levels in healthy donors (HD), patients with glandular (gl.) and extraglandular (egl.) pSS and SLE 2/A. 2/A Comparison.
Serum osteopontin (OPN) levels in population-based controls and in cases with SLE. Serum levels of OPN, determined by ELISA, were significantly higher.
Correlations of EBV-specific T-cells and disease activity of SLE patients. Correlations of EBV-specific T-cells and disease activity of SLE patients. Correlation.
The association between alcohol consumption and the severity of MRI-detected inflammation in hand and foot joints of (A) patients with RA and (B) asymptomatic.
Representative ultrasound images of patients with SLE
No difference in T-cell response between SLE patients and healthy controls upon superantigen stimulation. No difference in T-cell response between SLE.
Mean (SD) AMG 557 serum concentration–time profiles following single-ascending dose (SAD) (A) and multiple-ascending dose (MAD) (B) administration AMG.
Receiver operating curve of soluble C3, C4, antibodies to double-stranded DNA (anti-dsDNA) compared with complement C4d levels on erythrocytes (EC4d) and.
Longitudinal changes in serum G3BP concentrations and SLEDAI in 15 patients with SLE. Each plot represents one patient. Longitudinal changes in serum G3BP.
Performance characteristics for multivariate assay SLE panel.
Positivity rate for antibodies to double-stranded DNA (anti-dsDNA), low complement, high complement C4 activation products (CBCAPS) and two-tiered methodology.
Study schemas. Study schemas. Upper panel: single-ascending dose study. Subjects with mild, stable systemic lupus erythematosus (SLE) were randomised to.
Anifrolumab does not elicit antibody-dependent cell-mediated cytotoxicity (ADCC) or complement-dependent cytotoxicity (CDC) activity. Anifrolumab does.
Correlation between frequency of Th17 cells and disease activity or amount of proteinuria in patients with systemic lupus erythematosus (SLE). Correlation.
Correlation between mean Safety of Estrogens in Lupus Erythematosus National Assessment–Systemic Lupus Erythematosus Disease Activity Index (SELENA-SLEDAI)
Post-test probabilities of systemic lupus erythematosus (SLE) at different pretest probabilities for a positive and negative cell-bound complement activation.
Correlations between two measures of type I interferon activity and serum galectin-3-binding protein in the SLE-IFN-α (n=26) and HC-IFN-α (n=10) cohorts.
The effect of purified IgG from healthy controls or patients with lupus nephritis on tyrosine phosphorylation in podocytes at two different IgG concentrations.
Serum proteins dysregulated at baseline in patients enrolled in the MUSE study subsetted by IFNGS test status, Cutaneous Lupus Erythematosus Disease Area.
Complement and antibody abnormalities at baseline and relation to disease activity clinical SELENA-SLEDAI (A) and PGA scores (B) in relation to the presence.
First-generation modular analysis of acutely ill systemic lupus erythematosus (SLE) (flare or infection) versus inactive SLE. The modules are numbered;
Tyrosine phosphorylation of proteins in podocyte lysates following exposure to healthy or lupus nephritis plasma. Tyrosine phosphorylation of proteins.
Attributed cause of end-stage renal disease (ESRD) among 251 patients with SLE in the Georgia Lupus Registry who progressed to ESRD (1979–2012), overall.
Comparison of the effects of growing podocytes in plasma from patients with lupus nephritis (LN), rheumatoid arthritis or non-renal lupus. Comparison of.
Hierarchical clustering of non-classical monocytes from patients and controls, with tracks indicating individuals, IFN score, SLEDAI score and prednisone.
Representative example of gating on T-cell subpopulations.
Distribution of the RAMRIS component scores sorted by pain score.
Association of MRI findings and serum autoantibodies in diffuse neuropsychiatric systemic lupus erythematosus. Association of MRI findings and serum autoantibodies.
CD151 effects on mammary cell morphology and adhesion.
SLE deconvolution patient clusters and representative immune cell types (A), and distribution of patients by SLE deconvolution cluster and treatment group—all.
Multivariate assay panel for systemic lupus erythematosus (SLE) diagnosis. Multivariate assay panel for systemic lupus erythematosus (SLE) diagnosis. Two-tier.
Least squares (LS) mean (SE) changes from baseline in (A) Cutaneous Lupus Erythematosus Disease Area and Severity Index activity scores and (B) Tender.
Antibody levels to Ro52, Ro60, p200 and La antigens in control and congenital heart block (CHB) cohort were measured as bound units (BU). Antibody levels.
Proportion of patients consulting their general practitioner for symptoms within each British Isles Lupus Activity Group (BILAG) domain in the 5 years.
Heterogeneity of TCRβ repertoire in autoimmune diseases.
Immune cell populations associated with type I IFNGS test status and disease activity. Immune cell populations associated with type I IFNGS test status.
Impact of skin damage on health-related quality of life.
Fig. 3 BMS blocks functional responses in primary immune cells driven by IL-23 and IL-12. BMS blocks functional responses in primary immune.
Serum anti-neuronal antibodies (anti-N) in patients with positive serum anti-GRP78. Serum anti-neuronal antibodies (anti-N) in patients with positive serum.
Number of microparticles (MPs) and distribution of MP surface markers in patients with SLE and HCs. Three aliquots of MPs were incubated with (1) anti-CD3,
Mean fluorescence intensity (MFI) of SIGLEC1 expression before and after introduction of prednisolone or hydroxychloroquine. Mean fluorescence intensity.
Plots showing the difference in expression rate versus the difference in averaged transcript amount between patients with SLE with SLEDAI ≥10 and those.
Mean change from baseline over time in BILAG score,
Overall gene expression in monocyte subsets in patients and controls.
Fig. 4 Prematurely short S-phase and replication-associated DNA damage in p57KIP2-deficient fetal liver. Prematurely short S-phase and replication-associated.
Melanoma patient monocytes have altered expression of inflammatory and surface markers. Melanoma patient monocytes have altered expression of inflammatory.
(A) Mean urine protein/creatinine ratio (UPCR) and SEM in participants from the combined Lupus Nephritis Assessment of Rituximab (LUNAR) and A Study to.
IFN-γ-producing T-cells in SLE patients and healthy controls upon EBV antigen stimulation. IFN-γ-producing T-cells in SLE patients and healthy controls.
Activated T-cells in SLE patients and healthy controls upon EBV antigen stimulation. Activated T-cells in SLE patients and healthy controls upon EBV antigen.
Increased numbers of LDGs in association with disease activity and low complement levels in patients with SLE. Numbers of LDGs were determined by flow.
Abnormal monocyte distribution and loss of HLA-DR in patients with stage IV melanoma. Abnormal monocyte distribution and loss of HLA-DR in patients with.
Mice with a B cell–specific loss of Ets1 have reduced marginal zone B cells and increased ASCs. (A) Flow cytometry analysis of CD21 versus CD23 in gated.
Median percentage change in complement components 3 and 4 over time by SLE deconvolution cluster—all randomised and treated patients.* *Data from five.
TLR9 deficiency leads to more severe impairment of endothelium-dependent vasorelaxation and promotes aberrant B cell phenotype in imiquimod-induced autoimmunity.
Measures of endothelial activation/dysfunction are associated with QRISK3. Measures of endothelial activation/dysfunction are associated with QRISK3. Increased.
Fig. 3. Association between peak CTL019 expansion and response.
Changes in non-classical (CD11b+CD14+CD163−CD16+) and classical (CD11b+CD14+CD163+CD16−) monocytes over time in patients with rheumatoid arthritis (RA)
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(A) Phospho-H2AX levels are significantly increased in CD4+ T cells, CD8+ T cells and monocytes from SLE compared with those from healthy controls (p=2.16×10−4, 1.68×10−3 and 4.74×10−3, respectively) and RA (p=1.05×10−3, 1.78×10−3 and 2.43×10−2, respectivel... (A) Phospho-H2AX levels are significantly increased in CD4+ T cells, CD8+ T cells and monocytes from SLE compared with those from healthy controls (p=2.16×10−4, 1.68×10−3 and 4.74×10−3, respectively) and RA (p=1.05×10−3, 1.78×10−3 and 2.43×10−2, respectively). (B) Phospho-H2AX levels at G0/G1, S and G2 cell-cycle phases are significantly increased in CD3+ T cells in SLE compared with healthy controls (p=5.41×10−3, 9.71×10−3 and 2.86×10−3, respectively). In monocytes, there was a significant difference at G0/G1 and G2 cell-cycle phases (p=3.85×10−2 and 3.90×10−2, respectively), but the difference did not reach statistical significance at S phase (p=8.38×10−2). Phospho-H2AX levels were measured by flow cytometry, and are provided as MFIs (mean±SEM). HC, healthy controls; MFI, median fluorescence intensity; Phospho-H2AX, phosphorylated H2AX; RA, rheumatoid arthritis; SLE, systemic lupus erythematosus. Rajaie Namas et al. Lupus Sci Med 2016;3:e000148 ©2016 by Lupus Foundation of America