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(A) Serum IgM ... (A) Serum IgM anti-phosphorylcholine (PC) antibodies were diminished in SLE patients (n = 197) compared with controls (n = 99) [60.53.

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Presentation on theme: "(A) Serum IgM ... (A) Serum IgM anti-phosphorylcholine (PC) antibodies were diminished in SLE patients (n = 197) compared with controls (n = 99) [60.53."— Presentation transcript:

1 (A) Serum IgM ... (A) Serum IgM anti-phosphorylcholine (PC) antibodies were diminished in SLE patients (n = 197) compared with controls (n = 99) [60.53 (110.10) vs (98.71) arbitrary units (AU); P < 0.001]. (B) IgM anti-PC levels (in arbitrary units) in SLE according to the presence (+) or absence (−) of anti-dsDNA (53.01 vs ), anti-Smith antibodies (anti-Sm) (31.14 vs 62.60), anti-ribosomal P proteins antibodies (anti-RibP) (35.49 vs 63.14) or glucocorticoid treatment (20.86 vs 39.26). SLE IgM anti-PC levels were negatively correlated with BMI, disease duration and age. (C) Correlation of IgM anti-PC and lipid serum levels in patients and controls. Horizontal lines in scatter plots represent the median and interquartile range. Statistical significance was assessed by the Mann–Whitney U-test and Spearman’s rank correlations; IgM anti-PC levels were log<sub>10</sub>-transformed only for graphical representation. Unless provided in the caption above, the following copyright applies to the content of this slide: © The Author(s) Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For permissions, please article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model ( Rheumatology (Oxford), kez264, The content of this slide may be subject to copyright: please see the slide notes for details.

2 Fig. 2 IgM anti-phosphorylcholine antibodies and CD4+ T cell subsets in controls and SLE patients in the ... (A) Serum IgM anti-phosphorylcholine (PC) antibodies in a subgroup of controls (n = 33) and SLE patients (n = 120) classified by the presence of traditional cardiovascular risk factors (tCVR, n = 31), subclinical atheromatosis (sub-CVD, n = 30) or cardiovascular disease (CVD, n = 18). (B) Frequency and representative dot plots of CD4<sup>+</sup>CD28<sup>null</sup>, IL-17<sup>+</sup>Foxp3<sup>+</sup>, Th17 and Treg cells in controls and patients presenting tCVR, sub-CVD or CVD. (C) Correlation of IgM anti-PC serum levels and T cell frequencies in SLE according to their lipid profile. Horizontal lines in scatter plots represent the median and interquartile range; statistical differences were assessed by Kruskal–Wallis and Mann–Whitney U-tests (*P<0.05, **P<0.01, ***P<0.001) and Spearman’s rank correlations; IgM anti-PC levels were log<sub>10</sub>-transformed only for graphical representation. Unless provided in the caption above, the following copyright applies to the content of this slide: © The Author(s) Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For permissions, please article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model ( Rheumatology (Oxford), kez264, The content of this slide may be subject to copyright: please see the slide notes for details.

3 Fig. 3 Circulating levels of cytokines and their association with IgM anti-phosphorylcholine antibodies in controls ... (A) Serum levels of cytokines in controls and SLE patients. Horizontal lines in scatter plots represent the median and interquartile range. Differences between groups were evaluated by the Mann–Whitney U-test. Correlation of IgM anti-phosphorylcholine (PC) and cytokine serum levels in controls (B) and SLE patients (C) (only statistically significant correlations have been represented). Correlation analyses were evaluated by Spearman tests using non-transformed variables (IgM anti-PC levels were log<sub>10</sub>-transformed only for the graphical representation). Unless provided in the caption above, the following copyright applies to the content of this slide: © The Author(s) Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For permissions, please article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model ( Rheumatology (Oxford), kez264, The content of this slide may be subject to copyright: please see the slide notes for details.


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