TNF Intracellular staining in CD14 positive monocytes from healthy control and RA patients.

<p>A) Thawed A) Cryopreserved PBMC from control and RA patients were stimulated for 4hrs with LPS (1 µg/ml), heat-aggregated Ig [HAG] (100 µg/ml) or the absence of stimulation (NS). Representative dot plots/histograms are shown for all treatments in a HC individual and for HAG stimulation in a RA patient (bottom panel). Intracellular staining was performed using anti-human TNF-PE or isotype control-PE antibodies and MFI units of expression measured. B) Intracellular staining for TNF in response to LPS (left panel) and HAG (right panel) in healthy control (HC, n = 8) and RA (n = 15) subjects. C) Correlation between HAG-stimulated TNF intracellular staining and % CD16 positive monocytes in RA patients. The percentage of CD14⁺⁺ monocytes expressing CD16 (x-axis) and the MFI of anti-TNF-PE expression (y-axis) were determined by flow cytometry. Open diamonds represent early RA patient and shaded diamonds represent long-standing RA patients. Correlation coefficient spearman's rho = 0·813, p<0.001.</p

Early RA patient baseline demographics and associations with response to steroid/methotrexate therapy.

<p>A cohort of early RA patients (n = 73) were recruited for investigation. Baseline characteristics of the cohort is summarised in column [Entire cohort]. Patients with EULAR response data at week 14 post-initiation of therapy (n = 42) were furthermore split into non-responders [NR] or moderate/good responders [MOD/GOOD] and baseline characteristics in each subgroup analysed separately. Statistically significant differences between the two EULAR response subgroups [NR vs. MOD/GOOD] were examined. (‡) fishers statistical test (φ) mann-whitney U test.</p

FcγRIIIa/CD16 expression on RA CD14⁺⁺ monocytes pre- and post- methotrexate therapy.

<p>A) The percentage of CD16 positive CD14⁺⁺ monocytes was measured at baseline (y-axis) and correlated with patient responses to methotrexate treatment. Patients were classified at week 14 post-initiation of therapy as non-responders (NR, n = 12), moderate (MOD, n = 12) or good (GOOD, n = 15) according to EULAR criteria and compared using Mann Whitney U test. Dots represent outliers. (B) The percentage reduction in DAS28-ESR between 0 and 14 weeks post-initiation of therapy (x-axis) and the % of CD14⁺⁺ cells expressing CD16 at baseline (y-axis). Negative levels indicate increased DAS28ESR between baseline and week 14. Statistics; Spearman's correlation. C) The percentage of CD16 positive CD14⁺⁺ monocytes was measured at baseline (wk0), 2 and 14 weeks after initiation of steroid/methotrexate treatment in early DMARD-naïve RA patients. Samples at 2 weeks mainly reflect influence of steroid treatment whereas week 14 samples will mainly reflect the effect of methotrexate therapy. Wilcoxon signed ranks test used to compare paired samples pre- and post- therapy.</p

Risk categorisation of RA and controls by each prediction model.

<p>The y-axis on each graph refers to the proportion of cases/controls in each risk category; cont = controls; sero+ = seropositive RA; ACPA+ = ACPA-positive RA.</p

Non-HLA RA susceptibility SNP allele frequencies and their association with seropositive RA in WTCCC and UKRAGG.

<p>SNPs are ordered by significance (most significant by <i>P</i>_GWAS listed first); all alleles attained genome-wide significance in the published meta-analysis; Ca = Cases; Co = Controls; MAF = Minor Allele Frequency;</p>a<p> = MAF in controls.</p

Clinical characteristics of WTCCC/UKRAGG cases and controls included in modelling.

<p>Data are number (%) unless otherwise stated. The following data are missing from WTCCC: gender in 2 cases and 169 controls; RF status in 5 cases; ACPA status in 290 cases; age of onset missing/inaccurate in 63 cases; erosive status in 96 cases; smoking status in 76 male cases, 204 female cases and 3 female controls. The following data are missing from UKRAGG: gender in 14 controls; RF status in 60 cases; ACPA status in 844 cases; age of onset missing/inaccurate in 93 cases; erosive status in 1,432 cases; nodular status in 378 cases; smoking status in 226 male cases, 513 female cases, 274 male controls and 284 female controls.</p>a<p> = % of males that are ever smokers;</p>b<p> = % of females that are ever smokers.</p

Number of individuals evaluated in each prediction model.

<p>Number of individuals evaluated in each prediction model.</p

Prediction model generated risk profiles for ACPA-positive RA and controls.

<p>Panel A = WTCCC; Panel B = UKRAGG; the upper set of lines for each model refer to RA cases; the lower set of lines refer to controls; OR = odds ratio.</p

Kaplan-Meier curves: RA age of onset stratified by HLA model risk categorisation and smoking status.

<p>Panel A = WTCCC Curves Stratified By Risk Categorisation; Panel B = UKRAGG Curves Stratified By Risk Categorisation; Panel C = WTCCC Curves Stratified By Risk Categorisation and Ever-Smoking Status; Panel D = UKRAGG Curves Stratified By Risk Categorisation and Ever-Smoking Status; Δ = change in onset age; Δ_m = maximum change in onset age across strata.</p

Copy number of which is associated with systemic lupus erythematosus, correlates with protein expression and immune complex uptake-5

plate are shown (all of the raw data are shown in Fig. S1, A and B). The horizontal bar indicates the mean. The P values shown indicate comparison of all cases and controls using a stratified Student's test. (A) UK SLE patients, = 171; UK controls, = 176. (B) Hong Kong SLE patients, = 159; Hong Kong controls, = 150.<p><b>Copyright information:</b></p><p>Taken from "Copy number of which is associated with systemic lupus erythematosus, correlates with protein expression and immune complex uptake"</p><p></p><p>The Journal of Experimental Medicine 2008;205(7):1573-1582.</p><p>Published online 7 Jul 2008</p><p>PMCID:PMC2442635.</p><p></p