Common variable immunodeficiency (CVID) and specific antibody deficiency (SAD) are both inborn errors of immunity and thus thought to have a genetic basis. However, protein-coding mutations are associated with only 15-30% of CVID cases, and no association has yet been reported for SAD. While this suggests the existence of other, non-coding, mechanisms that might be at play, a comprehensive characterisation of the molecular features of these two immune disorders is still lacking. We have started analysing a multi-omics (CITE-seq) dataset of 392,269 single cells that we generated from PBMC samples obtained from 30 patients from 3 cohorts (ie, healthy, SAD and CVID). We used our dataset to start investigating cell type-frequency and gene expression differences across cohorts and individuals. More importantly, we also quantified the expression of DNA-regulatory elements, e.g., enhancers, from our single-cell transcriptomics data and used that to compare the activity of such elements across cohorts.