Blood proteins have provided essential insights into how humans responded to the recent pandemic. To expand our understanding beyond patients seeking medical care, we conducted a citizen-centric survey with 2,000 random residents (age: 18–69 years) from Sweden's two largest cities in 2021. With self-sampled dried blood spots (DBS) and health information from 437 (22%) volunteers, we performed multi-analyte COVID-19 serology, measured autoantibodies (AAbs) against 22 interferons, and quantified 502 circulating low-abundant immune-related blood proteins. Antibody assays confirmed self-reported infections (26%) and vaccinations (40%), showed timing-dependent discrepancies in the immune response, and revealed anti-type I interferon AAbs co-occurring frequently alongside natural infections. Proteomics data added plausible mechanistic insights into cell-mediated processes: data-driven analyses revealed 24% of participants presented deviating immune phenotypes linked to infections, immunity, respiratory effects, and age. Multi-molecular DBS analysis of random layperson samples captured the broader spectrum of immune system states, adding relevant insights for clinical and public health investigations.

Objectives: Triple-negative breast cancer (TNBC) is a highly aggressive breast cancer subtype with limited treatment options. Unlike other breast cancer subtypes, the scarcity of specific therapies and greater frequencies of distant metastases contribute to its aggressiveness. We aimed to find epigenetic changes that aid in the understanding of the dissemination process of these cancers. Data description: Using CRISPR/Cas9, our experimental approach led us to identify and disrupt an insulator element, IE8, whose activity seemed relevant for cell invasion. The experiments were performed in two well-established TNBC cellular models, the MDA-MB-231 and the MDA-MB-436. To gain insights into the underlying molecular mechanisms of TNBC invasion ability, we generated and characterized high-resolution chromatin interaction (Hi-C) and chromatin accessibility (ATAC-seq) maps in both cell models and complemented these datasets with gene expression profiling (RNA-seq) in MDA-MB-231, the cell line that showed more significant changes in chromatin accessibility. Altogether, our data provide a comprehensive resource for understanding the spatial organization of the genome in TNBC cells, which may contribute to accelerating the discovery of TNBC-specific alterations triggering advances for this devastating disease.