Fig. 5: CD11c+ B cells from individuals with DS are more prone to autoreactivity.
From: Autoimmunity in Down’s syndrome via cytokines, CD4 T cells and CD11c+ B cells

a,b, Expression of IgD (a) and IgA (b) in naive, CD11c+ and memory B cells and plasmablasts from adults with DS and age-matched HC individuals. n = 3 each. c–h, BCR sequencing analysis of genomic DNA isolated from sorted naive, CD11c+ and memory B cells from controls (n = 6) and individuals with DS (n = 6). c, The fraction of productive BCRs represented more than once in each sample. Individuals from whom a sample had fewer than 1,000 productive templates were excluded. d, CDR3 length of productive BCRs in B cells subsets in HC and DS, expressed as the number of nucleotides (nt). e, The mean number of nucleotides different from reference in the V gene of productive BCRs in B cells subsets in HC and DS. f, The frequency of productive BCRs that were aligned to the IGHV4-34 gene in each sample. g, 9G4 surface expression in naive, CD11c+ and memory B cells from HC individuals (n = 3) and individuals with DS (n = 3). h, ELISA quantification of 9G4 antibodies in the plasma of HC individuals (n = 8), and individuals with DS in the low/medium (n = 7) and high (n = 5) cytokine groups, expressed as the fold change over HC individuals. OD490, optical density at 490 nm. For a, b, g and h, data are mean ± s.d. For d–f, the whiskers denote the minimum and maximum values, the box limits denote quartile 1 to quartile 3, and the centre bar denotes the mean. Significance in a and h and significance between cell subsets in d was assessed using one-way ANOVA with Tukey’s post-hoc analysis. Significance in d–g between the HC and DS groups was assessed using two-tailed paired t-tests.