Swirski, Filip, PhD
Dr. Swirski is Associate Professor at Harvard Medical School (HMS) and Massachusetts General Hospital (MGH). In 2004, Dr. Swirski obtained his PhD in Immunology from McMaster University in Canada. In 2007, he completed his postdoctoral studies in Vascular Biology at Brigham and Women’s Hospital (BWH) and MGH, and was recruited to the Center for Systems Biology (CSB) at MGH and HMS. Dr. Swirski has received awards from the Canadian Institutes of Health Research (CIHR) and the American Heart Association (AHA). Currently, his research is supported by grants from the National Institutes of Health (NIH). Dr. Swirski studies innate immunity and leukocyte communication. Dr. Swirski is a member of the Harvard Immunology Ph. D. Program.
Selected Publications (from total of 134)
On-demand erythrocyte disposal and iron recycling requires transient macrophages in the liver
Interleukin-3 amplifies acute inflammation and is a potential therapeutic target in sepsis.
Pleural innate response activator B cells protect against pneumonia via a GM-CSF-IgM axis.
Ly-6Chigh Monocytes Depend on Nr4a1 to Balance both Inflammatory and Reparative Phases in the Infarcted Myocardium.
Innate Response Activator B Cells Aggravate Atherosclerosis by Stimulating TH1 Adaptive Immunity.
Local proliferation dominates lesional macrophage accumulation in atherosclerosis
Leukocyte behavior in atherosclerosis, myocardial infarction, and heart failure.
Innate Response Activator B Cells Protect Against Microbial Sepsis
Extramedullary Hematopoiesis Generates Ly-6Chigh Monocytes that Infiltrate Atherosclerotic Lesions.
Monocytes: protagonists of infarct inflammation and repair after myocardial infarction.
Identification of Splenic Reservoir Monocytes and Their Deployment to Inflammatory Sites
The healing myocardium sequentially mobilizes two monocyte subsets with divergent and complementary functions.
Ly-6Chi monocytes dominate hypercholesterolemia-associated monocytosis and give rise to macrophages in atheromata
Monocyte accumulation in mouse atherogenesis is progressive and proportional to extent of disease.