Fig. 9: Frequency, clonal sizes and phenotypes are different between HD- and T1D-derived GAD clonotypes.
From: Physiological and pathogenic T cell autoreactivity converge in type 1 diabetes
a, c Frequency of GAD-specific TCRB CDR3 amino acid clonoytpes in TN (a) and CM (c) peripheral immune repertoires, disaggregated by type of donor (57 clonotypes for HD, 90 for T1D and 64 for CMV). Shown are Tukey boxplots: boxes are interquartile range (25% to 75%), whisker (up) is 75th percentile plus 1.5 times the interquartile range (IQR). The centre is the 50th percentile. Individual dots are values that are greater than the whisker. Two-sided Mann Whitney U test with Bonferroni correction (***: p < 0.001). The frequency of each clonotype was calculated as the average frequency for all nucleotide sequences coding for the same amino acid sequence (See “Methods” section). b, d heatmaps showing the means of frequencies, and the corresponding p-values (two sided Mann Whitney U test with Bonferroni correction), of data shown in a, c. e, f we identified GAD clonotypes appearing in peripheral repertoires from HD but not from T1D patients (“HD-only”, in blue), and GAD clonotypes appearing in peripheral repertoires from T1D patients but not from HD (“T1D-only”, in red), and represented them on the UMAP space. GAD clonotypes found in TN repertoires are shown in (e), while those found in CM ones are shown in (f). Arrows in (e) depict expanded clonotypes. g HD-only (blue) and T1D-only (red) GAD clonotypes tracked into CM subsets which show clonal expansions.
