Anna Rydén, Maria Faresjö Diabetes Research and Clinical Practice

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Altered immune profile from pre-diabetes to manifestation of type 1 diabetes Anna Rydén, Maria Faresjö Diabetes Research and Clinical Practice Volume 100, Issue 1, Pages 74-84 (April 2013) DOI: 10.1016/j.diabres.2013.01.014 Copyright © 2013 Elsevier Ireland Ltd Terms and Conditions

Fig. 1 Description of study population; high-risk individuals, T1D children and healthy children and, study design including in vitro culture and detection of markers associated with regulatory T-cells (FOXP3, CTLA-4 and TGF-β mRNA) and immune markers associated with Th1, Th2, Tr1 and inflammatory cells (IL-1β, -6, -7, -10, -13, -17, IFN-γ, TNF-α, CCL2, -3, -4, -5 and CXCL10). Diabetes Research and Clinical Practice 2013 100, 74-84DOI: (10.1016/j.diabres.2013.01.014) Copyright © 2013 Elsevier Ireland Ltd Terms and Conditions

Fig. 2 Forkhead box protein P3 (FOXP3) (a) and cytotoxic T-lymphocyte associated protein 4 (CTLA-4) (b) mRNA expressions, following stimulation with Glutamic Acid Decarboxylase (GAD)65-protein and spontaneous CCL4 secretions (c) in high-risk individuals that stayed healthy versus those that later developed type 1 diabetes (T1D). Spontaneous secretion of interleukin (IL)-6 (d) and CCL3 (e) in high-risk individuals that had received nicotinamide treatment in comparison to those that received placebo. The bars in each figure correspond to the median values. *p<0.05. Diabetes Research and Clinical Practice 2013 100, 74-84DOI: (10.1016/j.diabres.2013.01.014) Copyright © 2013 Elsevier Ireland Ltd Terms and Conditions

Fig. 3 Spontaneous and mitogen (phytohaemagglutinin (PHA)) induced secretions of Tumour Necrosis Factor (TNF)-α (a and b) and the number of responders versus non-responders for TNF-α secretion in high-risk (c) and newly diagnosed type 1 diabetic (T1D) children (d), following PHA stimulation. The bars in each figure correspond to the median values. T1D 4d, newly diagnosed T1D children; T1D 8m, T1D children 8 months post diagnosis. *p<0.05, **p<0.01. Diabetes Research and Clinical Practice 2013 100, 74-84DOI: (10.1016/j.diabres.2013.01.014) Copyright © 2013 Elsevier Ireland Ltd Terms and Conditions

Fig. 4 CXCL10 (a) and CCL3 (b) secretions following stimulation with Glutamic Acid Decarboxylase (GAD)65-protein, heat shock protein (HSP)60-peptide (a.a. 437–460) induced secretions of CCL2 (c) and spontaneously secreted CCL5 (d). The bars in each figure correspond to the median values. T1D 4d, newly diagnosed T1D children, T1D 8m=T1D children 8 months post diagnosis. *p<0.05, **p<0.01. Diabetes Research and Clinical Practice 2013 100, 74-84DOI: (10.1016/j.diabres.2013.01.014) Copyright © 2013 Elsevier Ireland Ltd Terms and Conditions

Fig. 5 Spontaneous (a), glutamic acid decarboxylase (GAD)65-protein- (b) and phytohaemagglutinin (PHA) (c) stimulated forkhead box protein P3 (FOXP3) expression. The bars in each figure correspond to the median values. T1D 4d, newly diagnosed type 1 diabetic (T1D) children, T1D 8m, T1D children 8 months post diagnosis. *p<0.05, **p<0.01, ***p<0.001. Diabetes Research and Clinical Practice 2013 100, 74-84DOI: (10.1016/j.diabres.2013.01.014) Copyright © 2013 Elsevier Ireland Ltd Terms and Conditions