Effect of IL-6 deficiency on gene expression in cell types of control and HD mouse striatum

Huntington's disease (HD) is an incurable neurodegenerative disorder that is caused by CAG trinucleotide expansions in the huntingtin gene. However, the exact molecular and cellular mechanisms underlying the pathogenesis of HD are still not well understood. Immune signaling has been hypothesized to contribute to HD pathogenesis. In this study, we used single-nucleus RNA sequencing (snRNA-seq) to access the transcriptional profiles of striatal cell types in control and R6/2 HD model mice that either had normal levels of, or were deficient for, the cytokine interleukin-6 (IL-6). Our results provide insights into the gene expression programs that are under the control of this important immune regulator in both a normal and HD model context. Overall design: Single-cell profiling of Il6 knock-out spiny projection neurons in R62 mouse model of HD.