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We seek to understand the immunology that underlies lung inflammation and fibrosis in Interstitial Lung Disease (ILD). 

1. Unmet medical need in pulmonary fibrosis. An unappreciated blessing of good health is that breathing is unconscious and unnoticed. One of the worst parts of pulmonary medicine is seeing patients with lung fibrosis (“scarring”) becoming more and more short of breath. However, we have only two drugs for lung fibrosis, and these only modestly slow the rate of decline but do not cure. 

IPF and RA-ILD are fibrotic lung diseases with high rates of mortality. Idiopathic Pulmonary Fibrosis (IPF) has a median survival of only 3 years, worse than many cancers. Rheumatoid Arthritis-associated Interstitial Lung Disease (RA-ILD) affects 5-10% of RA patients. 

2. Our candidate drug targets and advantages.

1. Bedside to bench. Our lab is leveraging next generation technologies in single cell and spatial transcriptomics, bioinformatic analysis, and ex-vivo techniques in cell culture, to define the immunological mechanisms that govern the complex relationship between inflammation and fibrosis. By uncovering the cellular and molecular signatures that distinguish ILDs from one another, we can generate a more precise, immune based classification system that will help distinguish ILDs that are more inflammatory in nature, from those that progress to fibrosis and end stage lung disease. In turn, these discoveries can better inform current treatment options, as well as lead to the future development of more targeted and effective immunotherapies.

2. Autocrine loops in lung fibroblasts that are master amplifiers of inflammation and fibrosis. 
Advantage: Several clinical trials that tried to block on
ly one upstream stimulus have failed. We think blocking a downstream master amplifier is a better way to treat patients and reduces risk in therapeutic development. 


​3. T cell - fibroblast axes. Most of the lung fibrosis field does not focus on immunology. 
Advantage: We focus on unique mechanisms and have strong collaborations
in more inflammatory ILD (early ILD, RA-ILD). 


4. ​Lipid nanoparticle (LNP)/siRNA therapies (along with more traditional approaches like monoclonal antibodies).  

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