# Insights into the pathogenesis of rheumatic and immune diseases from single-cell omics

## TL;DR

This paper reviews how single-cell omics technologies are helping to uncover shared mechanisms in autoimmune diseases and guiding the development of targeted therapies.

## Contribution

The paper synthesizes recent single-cell omics findings across six autoimmune diseases and identifies shared pathological networks and therapeutic opportunities.

## Key findings

- Single-cell omics reveals core pathological networks shared across multiple autoimmune diseases.
- Mechanistic insights support cross-disease targeting using shared pathway interventions.
- Translational progress includes clinical activity of drugs like tofacitinib and abatacept across various autoimmune settings.

## Abstract

High-resolution, high-throughput single-cell omics has transformed our understanding of autoimmune disease pathogenesis. We synthesise recent single-cell omics advances across six autoimmune diseases—systemic sclerosis, systemic lupus erythematosus, Sjögren’s syndrome, ankylosing spondylitis, IgG4-related disease and rheumatoid arthritis. We further summarise translational progress in targeted therapies. We delineate core pathological networks shared across these conditions, highlight convergent mechanisms, and provide a mechanistic rationale for the clinical activity of agents such as tofacitinib and abatacept across multiple autoimmune settings. These insights support the feasibility of mechanism-informed, cross-disease targeting—deploying shared pathway interventions across distinct clinical entities. Finally, we discuss current technical and interpretative challenges and outline future directions for mechanistic discovery, target prioritisation and precision medicine.

Conceptual diagram illustrating how single-cell omics technologies such as ScRNA-seq, ScDNA-seq, ScATAC-seq, and spatial transcriptomics inform autoimmune disease mechanisms, leading to targeted drug therapies such as abatacept, baricitinib, tofacitinib, upadacitinib, belimumab, and rituximab.