Hierarchical clustering of non-classical monocytes from patients and controls, with tracks indicating individuals, IFN score, SLEDAI score and prednisone.

Slides:



Advertisements
Similar presentations
Proportion of patients that met the SRI-5 response criteria (A and C) and reasons for non-response (B and D) in trial 1 (A and B) and trial 2 (C and D).
Advertisements

Fig. 8. Recurrent copy number amplification of BRD4 gene was observed across common cancers. Recurrent copy number amplification of BRD4 gene was observed.
Anifrolumab inhibits type I interferon (IFN)-induced IFN-stimulated response element (ISRE) signalling. Anifrolumab inhibits type I interferon (IFN)-induced.
Time between systemic lupus erythematosus (SLE) and haematological malignancy diagnoses. Time between systemic lupus erythematosus (SLE) and haematological.
Host transcriptional profiling distinguishes patients with acute LRTI (LRTI+C+M) from those with noninfectious acute respiratory illness (no-LRTI). Host.
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.
Volume 72, Issue 7, Pages (October 2007)
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.
Immunohistochemistry staining of interferon (IFN)-λ in renal tissue.
Tfr cells’ transcriptomic profile distinguishes them from Treg and Tfh cells. Tfr cells’ transcriptomic profile distinguishes them from Treg and Tfh cells.
Bettina Heidecker et al. BTS 2016;1:
(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,
Patient organoids respond more diverse to drugs and with lower therapeutic potential than 2D cultured patient cells Patient organoids respond more diverse.
Figure 1 Reduced pedigrees of the 11 PFBC families with MYORG mutations. Arrow = proband; asterisk = DNA available; ... Figure 1 Reduced pedigrees of the.
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.
Transcriptome analyses of four regions of the mouse brain.
Network modules correspond to known and novel functional distinctions between neuronal subtypes. Network modules correspond to known and novel functional.
Deficiency of TLR9 promotes more severe renal inflammation in imiquimod-induced autoimmunity. Deficiency of TLR9 promotes more severe renal inflammation.
Volume 7, Issue 2, Pages (August 2010)
The identification of leucocyte subset-specific type 1 interferon (IFN-1) modules. The identification of leucocyte subset-specific type 1 interferon (IFN-1)
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.
Hierarchical clustering analysis of 7785 genes (genes with a log-ratio variation in the 25th centile and >5% missing data were excluded) (A) A heat map.
Serum osteopontin (OPN) levels in population-based controls and in cases with SLE. Serum levels of OPN, determined by ELISA, were significantly higher.
Immunohistochemistry (IHC) staining of interferon (IFN)-λ in renal tissue The figure demonstrates a repeated renal biopsy obtained from a patient after.
The distribution of lamin C and emerin in lymphoblastoid cell lines.
The effects of a dominant negative mutant of lamin B1 on lamin distribution in HeLa cells. The effects of a dominant negative mutant of lamin B1 on lamin.
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.
Fig. 2 Ro60 commensal bacteria are common among lupus and healthy subjects without overt dysbiosis of the fecal, oral, or skin microbiome. Ro60 commensal.
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.
Timelines used to identify symptoms recorded in the 5 years before SLE diagnosis taking into account data censoring. Timelines used to identify symptoms.
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.
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.
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;
Comparison of the effects of growing podocytes in plasma from patients with lupus nephritis (LN), rheumatoid arthritis or non-renal lupus. Comparison of.
Representative example of gating on T-cell subpopulations.
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.
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.
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.
A, unsupervised hierarchical clustering of the expression of probe sets differentially expressed in the oral mucosa of smokers versus never smokers. A,
Unsupervised clustering heat map of genome-wide mRNA expression profiles, using skin samples from 49 MF/SS patients and 3 healthy individuals. Unsupervised.
Mean change from baseline over time in BILAG score,
Heat map of microRNA microarray expression from the four groups of patients. Heat map of microRNA microarray expression from the four groups of patients.
Overall gene expression in monocyte subsets in patients and controls.
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.
Measures of endothelial activation/dysfunction are associated with QRISK3. Measures of endothelial activation/dysfunction are associated with QRISK3. Increased.
Distinct subtypes of CAFs are detected in human PDAC
Characteristic gene expression patterns distinguish LCH cells from other immune cells present in LCH lesions. Characteristic gene expression patterns distinguish.
(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:

Hierarchical clustering of non-classical monocytes from patients and controls, with tracks indicating individuals, IFN score, SLEDAI score and prednisone usage. Hierarchical clustering of non-classical monocytes from patients and controls, with tracks indicating individuals, IFN score, SLEDAI score and prednisone usage. Each single cell forms a single row, and each column corresponds to an individual gene. All non-classical cells and genes are shown. Lower right corner inset shows heat map colour scheme key, with units indicating the delta CT values for each transcript. Colour codes for the data columns: Subject—white: healthy subjects; each colour represents one subject with SLE; interferon (IFN) score—darker green means higher IFN score; systemic lupus erythematosus disease activity index (SLEDAI) score—red: SLEDAI ≥10; pink: SLEDAI 3 to 6; white: SLEDAI 0 to 2; prednisone—dark blue: 20 mg/day; light blue: less than 10 mg/day; white: no prednisone. Black horizontal bars demarcate groups of cells that correspond to controls, high IFN, high SLEDAI and high-dose prednisone. Zhongbo Jin et al. Lupus Sci Med 2017;4:e000202 ©2017 by Lupus Foundation of America