Immune cell populations associated with type I IFNGS test status and disease activity. Immune cell populations associated with type I IFNGS test status.

Slides:



Advertisements
Similar presentations
Anifrolumab inhibits cytokine production, plasmacytoid dendritic cell (pDC) activation and the type I (interferon gene signature) IFN gene signature. Anifrolumab.
Advertisements

Anifrolumab inhibits type I interferon (IFN)-induced IFN-stimulated response element (ISRE) signalling. Anifrolumab inhibits type I interferon (IFN)-induced.
Figure 3 Nucleic acid sensors in SLE
Time between systemic lupus erythematosus (SLE) and haematological malignancy diagnoses. Time between systemic lupus erythematosus (SLE) and haematological.
Time course for laboratory parameters of a patient with systemic lupus erythematosus prior and during bortezomib therapy (arrow). Time course for laboratory.
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.
Fig. 7. The PD-L1 defect is evident in HSPCs from T1D patients.
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.
Elevated regulatory T cells at diagnosis of Coccidioides infection associates with chronicity in pediatric patients  Dan Davini, BA, Fouzia Naeem, MD,
Mean Safety of Estrogens in Lupus Erythematosus National Assessment–Systemic Lupus Erythematosus Disease Activity Index (SELENA-SLEDAI) score at the last.
Immunohistochemistry staining of interferon (IFN)-λ in renal tissue.
(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,
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.
Association of pretreatment interferon (IFN) signature metric (ISM) status with serum autoantibodies, BAFF levels and type I IFN bioactivity. Association.
Deficiency of TLR9 promotes more severe renal inflammation in imiquimod-induced autoimmunity. Deficiency of TLR9 promotes more severe renal inflammation.
The identification of leucocyte subset-specific type 1 interferon (IFN-1) modules. The identification of leucocyte subset-specific type 1 interferon (IFN-1)
Fig. 5 Extended local release of R848 increases the number of innate and adaptive antitumor immune cells and cytokines. Extended local release of R848.
Association of B cell TLR4 levels to disease activity.
Fig. 5 Treatment with an OX40 agonist antibody of 3-week-old HBVtgRag−/− mice or mice with chronic HBV disease results in an altered immune response to.
Figure 2 CD4+ T-cell subsets fluorescence-activated cell sorting analysis in peripheral blood mononuclear cells of patients with multiple sclerosis treated.
Serum osteopontin (OPN) levels in population-based controls and in cases with SLE. Serum levels of OPN, determined by ELISA, were significantly higher.
Forest plot of CIMT progression rate for atorvastatin treatment versus placebo for 3 years by baseline serum 25-hydroxyvitamin D status. Forest plot of.
Immunohistochemistry (IHC) staining of interferon (IFN)-λ in renal tissue The figure demonstrates a repeated renal biopsy obtained from a patient after.
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.
PD-L1 selectively marks circulating NCMs.
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.
Anifrolumab does not elicit antibody-dependent cell-mediated cytotoxicity (ADCC) or complement-dependent cytotoxicity (CDC) activity. Anifrolumab does.
Effects of DWJM on UCB CD34+-derived cell subsets.
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.
Urinary cell casts, lymph node weights and proteinuria in the lpr-water, lpr-CU and lpr-TU groups of mice. Urinary cell casts, lymph node weights and proteinuria.
CD4+CLA+CD103+ T cells from human blood and skin share a transcriptional profile. CD4+CLA+CD103+ T cells from human blood and skin share a transcriptional.
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;
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.
The role of IFN in viral infection over time
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.
Association of MRI findings and serum autoantibodies in diffuse neuropsychiatric systemic lupus erythematosus. Association of MRI findings and serum autoantibodies.
Presence of inpatient diagnostic codes for attributed cause of end-stage renal disease (ESRD) among 46 patients with systemic lupus erythematosus (SLE)
SLE deconvolution patient clusters and representative immune cell types (A), and distribution of patients by SLE deconvolution cluster and treatment group—all.
Least squares (LS) mean (SE) changes from baseline in (A) Cutaneous Lupus Erythematosus Disease Area and Severity Index activity scores and (B) Tender.
Proportion of patients consulting their general practitioner for symptoms within each British Isles Lupus Activity Group (BILAG) domain in the 5 years.
Impact of skin damage on health-related quality of life.
Overexpression of IL-27 upregulates expression of multiple IR by T cells in vivo. Overexpression of IL-27 upregulates expression of multiple IR by T cells.
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,
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,
The role of IFN in viral infection over time
Overall gene expression in monocyte subsets in patients and controls.
(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.
Changes over time in DAS 28 (A), SLEDAI (B), glucocorticoid dose (C) and EULAR response (D) in patients with rhupus treated by anti-TNF-α. Box plot (median,
Median percentage change in complement components 3 and 4 over time by SLE deconvolution cluster—all randomised and treated patients.* *Data from five.
(A–E) demonstrate a kidney biopsy from a patient with lupus nephritis (LN) class V. Representative micrographs: (A), an inflammatory infiltrate with T.
Presentation transcript:

Immune cell populations associated with type I IFNGS test status and disease activity. Immune cell populations associated with type I IFNGS test status and disease activity. Data are mean fold change of baseline flow cytometry measurements±95% CIs of immune cell subsets in IFNGS test-high versus IFNGS test-low patients, patients with Cutaneous Lupus Erythematosus Disease Area and Severity Index (CLASI) ≥10 versus patients with CLASI <10, and patients with Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) ≥10 versus patients with SLEDAI <10. A constant value of 0.5 was added to all data points before a log2 transformation was applied. Statistical analysis was carried out using a Student’s t-test. Significant p-values <0.05 are reported. DC, dendritic cells; IFN, interferon; IFNGS, IFN gene signature; n.s., not significant; WB, whole blood; WBC, white blood cells. Kerry A Casey et al. Lupus Sci Med 2018;5:e000286 ©2018 by Lupus Foundation of America