Fig. 8: GAD-specific TCRB CDR3 amino acid clonotypes from T1D patients show differential publicity and convergence features within peripheral immune repertoires.
From: Physiological and pathogenic T cell autoreactivity converge in type 1 diabetes
a, b: Percentage of peripheral immune repertoires where each GAD-specific TCRB CDR3 amino acid clonotype is tracked into, disaggregated per type of subject (a HD, and b T1D). Orange shade: extremely public clonotypes (present in ≥ 75% of individuals). Pink shade: public clonotypes (present in 25.0%–74.9% of individuals). Green shade: private clonotypes (present in 3.23%–24.9% of individuals) or ultraprivate (only found in the same single-cell donor, 3.23%). For Treg and Tscm, the threshold for “ultraprivate” is 5.88 and 6.25 respectively (faint dotted lines). c Percentage of repertoires where GAD-specific TCRB CDR3 amino acid clonotypes are tracked back into (HD: 32 clonotypes into TN, 51 into CM, 23 into Treg and 10 into Tscm. T1D: 66 clonotypes into TN, 77 into CM, 29 into Treg and 25 into Tscm. Two-sided Mann-Whitney U test. *p = 0.013). Blue: HD. Red: T1D. d Proportions of each publicity-based clonotype category in Treg repertoires (two-sided Chi-square test. * p = 0.0025. Blue: HD. Red: T1D). e–h correlations between number of convergent nucleotide sequences and frequency for each GAD-specific TCRB CDR3 amino acid clonotype tracked back into peripheral immune repertoires (Spearman correlation). e, f correlations for GAD (e) and CMV (f) clonotypes found in TN subsets. g, h correlations for GAD (g) and CMV (h) clonotypes found in CM subsets. e, g Blue: HD-derived GAD clonotypes. Red: T1D-derived GAD clonotypes. Error bars represent standard deviations.
