This program supports basic, translational, observational, and pre-clinical studies on scleroderma, fibrosis, and autoinflammatory diseases.
Scleroderma is an autoimmune rheumatic disease without an available curative therapy. It is a heterogenous and complex disease that can be categorized as localized scleroderma (morphea) and systemic scleroderma. While etiology of scleroderma is poorly understood, abnormal vasculature, inflammation, and fibrosis are main characteristics of the disease with diverse clinical manifestations (e.g. Raynaud’s phenomenon, digital ulcers, fibrosis in skin and internal organs). Fibrosis is an exaggerated wound healing process which is characterized by a progressive scarring and hardening of tissues with excessive deposition of extracellular matrix. This program supports research on scleroderma, fibrotic diseases, and fibrotic comorbidities associated with rheumatic diseases (e.g. Interstitial lung disease).
Another axis of this program lies on research of autoinflammatory diseases and inflammasome biology. Autoinflammatory diseases are caused by defect(s) or dysregulation of the innate immune system, characterized by recurrent or continuous inflammation. Delineation of the mechanism and outcomes of inflammasome activation and cross-talk with other signaling pathways would be one of main focuses to better understand autoinflammatory diseases.
Within each of these portfolio areas, studies emphasize the followings:
- Molecular and cellular mechanisms of pathogenesis and pathophysiology
- Identification of unique genomic, epigenomic, and proteomic signatures
- Immune cells or non-immune cells (e.g. fibroblasts, endothelium, pericytes, and adipocytes) or cross-talk among these cells leading to impaired inflammation resolution, acute and chronic inflammation, and fibrosis
- Development of animal and organoid models
- Translational and pre-clinical research on diagnostic and therapeutic development