Association of pretreatment interferon (IFN) signature metric (ISM) status with serum autoantibodies, BAFF levels and type I IFN bioactivity. Association.

Slides:



Advertisements
Similar presentations
From: GCAP1, Rab6, and HSP27: Novel Autoantibody Targets in Cancer-Associated Retinopathy and Autoimmune Retinopathy Trans. Vis. Sci. Tech ;5(3):1.
Advertisements

Anifrolumab inhibits cytokine production, plasmacytoid dendritic cell (pDC) activation and the type I (interferon gene signature) IFN gene signature. Anifrolumab.
Figure 2 Cell-mediated disease mechanisms of lupus nephritis
Nat. Rev. Nephrol. doi: /nrneph
Anifrolumab inhibits type I interferon (IFN)-induced IFN-stimulated response element (ISRE) signalling. Anifrolumab inhibits type I interferon (IFN)-induced.
Figure 4 Antinuclear antibodies and disease activity in SLE
Time between systemic lupus erythematosus (SLE) and haematological malignancy diagnoses. Time between systemic lupus erythematosus (SLE) and haematological.
Nat. Rev. Rheumatol. doi: /nrrheum
(A) Proposed new ANA result interpretation algorithm that includes the anti-DFS70 results. (A) Proposed new ANA result interpretation algorithm that includes.
Time course for laboratory parameters of a patient with systemic lupus erythematosus prior and during bortezomib therapy (arrow). Time course for laboratory.
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.
Serum levels of angiopoietin-like protein 4 (ANGPTL4) according to patients with chronic obstructive pulmonary disease and controls without any lung disease.
A clinical overview of autoantibodies in general practice rheumatology
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.
Fig. 3. The effects of DCA on hemodynamic and functional end points and their association with genetic factors (variants of the SIRT3 and UCP2 genes) that.
(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,
Longevity of mucosal and systemic antibody responses induced by pulmonary vaccination. Longevity of mucosal and systemic antibody responses induced by.
Deficiency of TLR9 promotes more severe renal inflammation in imiquimod-induced autoimmunity. Deficiency of TLR9 promotes more severe renal inflammation.
Deficiency of TLR9 does not affect autoantibody levels but shifts autoantibody specificity. Deficiency of TLR9 does not affect autoantibody levels but.
Fig. 7 Vaccine-induced influenza-specific B cells are not maintained in peripheral blood. Vaccine-induced influenza-specific B cells are not maintained.
Fig. 1 Anti-LtxA antibody concentrations in various patient groups.
IIV induces CD21hiCD27+ and CD21loCD27+ influenza-specific B cells
Box plot showing median cytokine levels and IQRs for (A) IP-10, (B) TNF-α, (C) LT-α and (D) IFN-γ in controls and pSS fatigue groups. Box plot showing.
Core type 1 interferon (IFN-1)-associated genes are more highly expressed in myeloid subsets. Core type 1 interferon (IFN-1)-associated genes are more.
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.
No difference in T-cell response between SLE patients and healthy controls upon superantigen stimulation. No difference in T-cell response between SLE.
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.
Interleukin-1 blockade effects interferon (IFN)-γ production by multiple cell types. a) Gating strategy for flow cytometry: CD56+ natural killer (NK) cells.
Fig. 6. TIV-09, but not MIV-09, induces an IFN signature in the blood of vaccinated individuals at day 1. TIV-09, but not MIV-09, induces an IFN signature.
Anti-RNP/anti-Sm antibodies in sera (bleeds 1–5) and H&E stained sections of kidney/salivary gland of the MRL-lpr/lpr and MRL-MpJ mice provided with water,
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.
Celiac disease as a model for SLE
The effect of purified IgG from healthy controls or patients with lupus nephritis on tyrosine phosphorylation in podocytes at two different IgG concentrations.
Antinuclear antibody (ANA) patterns (using HEp-2 ANA assay kit) and anti-dsDNA (analysed by Crithidia luciliae assay) in sera of the lpr-water, lpr-CU.
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.
Tyrosine phosphorylation of proteins in podocyte lysates following exposure to healthy or lupus nephritis plasma. Tyrosine phosphorylation of proteins.
Change in urinary protein to creatinine ratio (uPCR) as a function of serum C4, C3, anti-C1q, EC4d, EC3d and ECR1. Change in urinary protein to creatinine.
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.
SLE deconvolution patient clusters and representative immune cell types (A), and distribution of patients by SLE deconvolution cluster and treatment group—all.
Anti-DNA Abs were not affected by the deletion of GCs in pristane-induced lupus model. Anti-DNA Abs were not affected by the deletion of GCs in pristane-induced.
Multivariate assay panel for systemic lupus erythematosus (SLE) diagnosis. Multivariate assay panel for systemic lupus erythematosus (SLE) diagnosis. Two-tier.
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.
Immune cell populations associated with type I IFNGS test status and disease activity. Immune cell populations associated with type I IFNGS test status.
Presence of autoreactive anti-HLA antibodies among SLE and RA subjects
BMS blocks functional responses in primary immune cells driven by IFNα
Serum anti-neuronal antibodies (anti-N) in patients with positive serum anti-GRP78. Serum anti-neuronal antibodies (anti-N) in patients with positive serum.
Plots showing the difference in expression rate versus the difference in averaged transcript amount between patients with SLE with SLEDAI ≥10 and those.
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.
Correlation of PTEN loss in melanoma cells with an immune resistance phenotype. Correlation of PTEN loss in melanoma cells with an immune resistance phenotype.
Mean serum concentration time profiles of anifrolumab following subcutaneous and intravenous administration of anifrolumab.a aData below the limits of.
Serial determinations of both anti-chromatin and anti-dsDNA antibodies in a patient who developed lupus nephropathy during the study period, showing that.
Median percentage change in complement components 3 and 4 over time by SLE deconvolution cluster—all randomised and treated patients.* *Data from five.
Fig. 1 Anti-LtxA antibody concentrations in various patient groups.
(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:

Association of pretreatment interferon (IFN) signature metric (ISM) status with serum autoantibodies, BAFF levels and type I IFN bioactivity. Association of pretreatment interferon (IFN) signature metric (ISM) status with serum autoantibodies, BAFF levels and type I IFN bioactivity. Patients with extrarenal lupus (ERL) from the rontalizumab Phase I and Phase IIa ROSE trials and from the rituximab EXPLORER trial were pooled and stratified by ISM-Low (n=118) or High (n=307) status. Patients with renal lupus from the rituximab LUNAR trial were also examined (ISM-Low n=21; ISM-High n=59). (A) Levels of anti-dsDNA antibodies plotted as median, IQRs, and 5th and 95th centiles. Statistical significance was determined using the Wilcoxon test. (B) Presence or absence of extractable nuclear antigen (ENA) antibodies plotted as percentages of the patient subgroups. Statistical significance was determined using Fisher's exact test. (C) Levels of serum BAFF plotted as median, IQRs, and 5th and 95th centiles. Statistical significance was determined using the Wilcoxon test. (D) Levels of serum myxovirus influenza resistance 1 (MX1)-induced bioactivity in ROSE patients with ERL are plotted as median, IQRs, and 5th and 95th centiles. Statistical significance was determined using the Wilcoxon test. William P Kennedy et al. Lupus Sci Med 2015;2:e000080 ©2015 by Lupus Foundation of America