Extended Data Fig. 3: Quantitative analysis of IgG binding to cardiac tissues and individual cells.

(a) Summary of Pearson correlation coefficients of clinical 18F-FDG uptake quantified as SUVs compared with corresponding patient IgG binding levels to engineered tissues in vitro (MFI, second row) and with other clinical data collected as part of the cohort. (b,c) IgG binding level quantification (measured by MFI) of IgG isolated from patients with low levels of myocardial inflammation (SUVmax < 10) and elevated myocardial inflammation (SUVmax > 10) to stressed and non-stressed hiPSC-cardiomyocytes (b) and healthy left ventricle (LV) tissue sample (c). n = 9 patients with SUVmax < 10, and n = 3 patients with SUVmax > 10; n = 8 fields of view per patient in (b) or n = 3 fields of view per patient in (c). (d) Flow analysis of IgG binding to live and apoptotic hiPSC-CMs (Apo + ), and live, non-apoptotic (Apo-) stressed and non-stressed hiPSC-CMs in the three cohort patients with elevated myocardial inflammation. n = 3 biological replicates per patient. (e-g) Sample gating strategy of Apotracker Green+ and IgG+ in stressed and non-stressed iPSC-CMs. Pseudocolor scatter plots of (e) unstained, unstressed hiPSC-CMs and (f) stressed hiPSC-CMs stained for Propidium Iodide (PI), Apotracker, and Alexa Fluor 647-conjugated anti-human IgG. (g) Histogram of IgG binding in stressed Apotacker+ (black), non-stressed Apotracker- (pink), or stressed Apotracker- (teal) hiPSC-CMs. (h) Example flow cytometry gating strategy used to identify live (PI-, Apotracker green-) hiPSC-CMs, shown in Q4. Data represented as mean ± s.e.m. Ordinary two-way ANOVA with Tukey’s test for multiple comparisons in (b,d) and unpaired two-tailed Student’s t-test in (c). **** p < 0.0001.