Idiopathic inflammatory myopathies (IIM)

Idiopathic inflammatory myopathies (IIM), including dermatomyositis and polymyositis, are rare autoimmune diseases characterized by muscle inflammation, weakness, and systemic complications. Our lab investigates IIM pathogenesis and develops precision therapies by integrating metabolomics of patient muscle samples, single-cell transcriptomic analyses, and multi-omics profiling. We explore mitochondrial transplantation as a regenerative therapy, revealing its potential to restore mitochondrial function and suppress inflammation. In parallel, we identify novel biomarkers and therapeutic targets, and distinct immune mechanisms between autoimmune diseases and cancer. Through cellular, animal, and clinical studies, we aim to clarify immune–muscle interactions, treatment response mechanisms, and ultimately accelerate the development of innovative therapies for inflammatory myopathies.

Ankylosing Spondylitis

Ankylosing spondylitis (AS) is a chronic, immune-mediated inflammatory arthritis that primarily affects the spine and sacroiliac joints . We collected peripheral blood mononuclear cells (PBMCs) from AS patients before and after TNFi treatment and applied longitudinal, multi-omics profiling, including single-cell RNA sequencing (scRNA-seq), bulk RNA-seq, ELISA-based protein quantification, and in vitro functional assays. We analyzed immune cell populations, gene expression changes, and cytokine signaling pathways to distinguish responders from non-responders. We revealed that elevated baseline type I interferon (IFN) signatures predict poor TNFi response and that, paradoxically, TNFi can enhance IFN signaling and Th17 responses in non-responders. We suggest that personalized treatment approaches considering AIF-1 levels and IFN signatures may improve the management of AS.