BIOPSII Core

PROJECT SUMMARY/ABSTRACT (BIOPSII Core) In the last few years, our ability to measure biological changes in cells and tissues has grown exponentially with the advent of single-cell and spatial technologies. Through single-cell and spatial integration, we are now capable of providing detailed biological information down to an individual cell level regarding gene expression, epigenetic regulation, and compartmentalization of disease processes. The BIOPSII core is part of the University of Michigan Integrated Program for Cutaneous Immune-Stromal Interactions in SLE (IPCISS) and will build upon an accomplished collaborative working group seeking to understand the etiologies of CLE and SLE. The BIOPSII core will leverage unique analytical capabilities that we have built up at the University of Michigan, including highly specialized analytical tools, unique and extensive datasets, along with cutting-edge infrastructure. The objective of the BIOPSII core is to support the research components outlined in Project 1 and Project 2 of the U-M IPCISS program. The specific aims of the BIOPSII Core are: Aim 1: Provide Data Warehouse and Processing Capabilities for the U-M IPCISS by deploying robust, standardized pipelines for processing of single-cell transcriptomic, chromatin accessibility, spatial transcriptomics, bulk RNA/ATAC/ChIP-seq, and genetic data. Aim 2: Deploy Data Analysis Pipelines to Advance Integration and Interpretation of Multimodal Datasets (single-cell RNA-seq/ATAC seq, epigenetic information, spatial information, and genetics) toward the construction of high-quality maps of inflammatory processes in systemic lupus erythematosus/cutaneous lupus erythematosus skin. Aim 3: Incorporation, Optimization, and Integration of Novel Technologies and Bioinformatic Tools for multi-omic data analysis. Through its support of the two U-M IPCISS projects, the BIOPSII Core will amplify the impact of the U-M IPCISS program and greatly accelerate progress toward a greater understanding of critical mechanisms driving lupus pathogenesis.