Genome-wide association studies (GWAS) have identified genomic regions associated with complex traits, but pinpointing the causal genes remains challenging due to context-specific genetic regulation. In this study, we integrate single-cell expression quantitative trait loci (sc-eQTL) data from 1,925 individuals in the TenK10K cohort1 with GWAS to map the putative causal associations between cell type-specific gene expression across 28 peripheral immune cell types and 100 complex traits, including 69 diseases and 31 biomarkers.
Using Mendelian randomization, we identified over 8,000 genes causally associated with at least one disease and over 16,000 with at least one biomarker, totaling 188,634 unique gene–trait associations. Of these, ~35% were undetectable by GWAS-only analysis and ~61% were not captured by bulk-tissue eQTL analysis. Associations that are found only by using sc-eQTL data were often restricted to a few cell types, highlighting the value of cell type-resolved sc-eQTL mapping. Further, we demonstrate associations of ZBTB38 expression in T and B cells with Crohn’s disease that match results from an external differential gene expression study2 using disease-affected intestinal tissue, providing insights into cellular mechanisms of disease.
Through polygenic enrichment analysis, we demonstrate that peripheral immune cell types were enriched for both immune-related and systemic diseases. We observed strong polygenic enrichment for immune-mediated diseases in dendritic cells. Notably, two sub-populations of these cells exhibited distinct enrichment patterns, differentiating between autoimmune disorders and viral infections.
We estimate that past clinical development programs3 with target–indication pairs supported by single-cell MR association identified in our study were 3.3 times more likely to reach regulatory approval, showing the translational potential of these results to accelerate drug development.
Our study demonstrates a framework to characterise cell type-specific effects of genes using single-cell genetics to advance understanding of causal disease biology and identify effective therapeutics targets at cellular level.