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Principal Investigator, Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital
Chief, Pulmonary and Critical Care Unit, Massachusetts General Hospital
Associate Director, Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital
Associate Physician, Massachusetts General Hospital
Associate Professor of Medicine, Harvard Medical School
The Medoff Laboratory studies the pathogenesis of pulmonary inflammation, specifically the role of T cells in mediating inflammatory lung diseases. Using genetically modified mice in various models of lung disease as well as studies in humans with asthma or after lung transplantation, we study mechanisms of T cell activation and function in the context of these disorders. As a result of this work, we hope to delineate some of the molecular mechanisms involved in the development of T cell-mediated inflammatory lung disease. In addition, we also hope to reveal novel aspects of T cell biology and potential therapeutic targets for these disorders.
Jason Griffith, MD, PhD
Dr. Medoff’s research projects focus on the pathogenic mechanisms of inflammatory lung disease, specifically the mechanisms of T cell-mediated pulmonary inflammation. Currently we are focusing on three projects:
Role of the CARMA proteins in asthma
We are investigating the role of the proteins CARMA1 and CARMA3 in the development of allergic airway inflammation. The CARMA proteins have been shown to be crucial for activation of the NF-kB family of transcription factors. Utilizing mice with genetic deletion or mutations of the genes for these proteins in murine models of asthma, we have begun to explore their role in the development of airway inflammation.
Role of Tim3 in T cell-mediated lung disease
T cells are critical to the development of lung transplant rejection. Thus the mediators that control T cell activity play a central role in the development of this disorder. T-cell immunoglobulin domain and mucin domain 3 (Tim3) is a protein expressed on Th1 cells that seems to have anti-inflammatory properties. In this project, we are investigating the importance of Tim3 in acute rejection in a murine model of lung transplantation.
Role of adiponectin in pulmonary vascular disease
Obesity is now recognized to be a pro-inflammatory state that increases the risk of diseases such as atherosclerosis and diabetes. More recently, it has become apparent that there is also an increased prevalence of pulmonary hypertension in obese individuals. Since adipose tissue is an important source of immune active proteins, it is thought that obesity may directly contribute to inflammation and vascular remodeling through secretion of both inflammatory and anti-inflammatory mediators. In this project, we are investigating the role of the adipocyte specific protein adiponectin, in the development of pulmonary vascular remodeling in a murine model of pulmonary hypertension.
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