Macrophages regulate tissue regeneration following injury. They can worsen tissue injury by producing reactive oxygen species and other toxic mediators that disrupt cell metabolism, induce apoptosis, and exacerbate ischemic injury. However, they also produce a variety of growth factors, such as IGF-1, VEGF-ÃŽÂ±, TGF-ÃŽÂ², and Wnt proteins that regulate epithelial and endothelial cell proliferation, myofibroblast activation, stem and tissue progenitor cell differentiation, and angiogenesis. Proresolving macrophages in turn restore tissue homeostasis by functioning as anti-inflammatory cells, and macrophage-derived matrix metalloproteinases regulate fibrin and collagen turnover. However, dysregulated macrophage function impairs wound healing and contributes to the development of fibrosis. Consequently, the mechanisms that regulate these different macrophage activation states have become active areas of research. In this presentation, I will discuss the common and unique mechanisms by which macrophages instruct tissue repair and regulate tissue fibrogenesis.
Department of Immunology and Division of Rheumatology, Mayo Clinic
National Institute of Allergy & Infectious Diseases
Dr. Wynn is a Senior Investigator and Chief of the Immunopathogenesis Section of the Laboratory of Parasitic Disease, in the National Institute of Allergy and Infectious Diseases, NIH in Bethesda, MD. His laboratory group uses in vivo model systems to elucidate the immunological mechanisms controlling chronic inflammation and fibrosis. He and his colleagues have published over 200 scholarly research papers, reviews, and book chapters in many prestigious journals including Nature, Nature Immunology, Immunity, Journal of Experimental Medicine, Gastroenterology, Nature Reviews Immunology, Science Translational Medicine, Nature Medicine, and Annual Review of Immunology. He has made seminal contributions to our understanding of the role of IL-13, IL-17A, and macrophages in the progression and resolution of fibrosis in various organ systems and has developed improved in vivo models to test novel anti-fibrotic drugs. More recently, his laboratory has investigated the role of macrophages, fibroblasts and tissue progenitor cells in tissue regeneration. Dr. Wynn was elected to fellowship in the American Academy of Microbiology and has received several prestigious awards including the Bailey K. Ashford Medal from the American Society of Tropical Medicine and Hygiene, the Oswaldo Cruz Medal from the Oswaldo Cruz Foundation. In 2015 and 2106 Thomson Reuters included him among their list of Highly Cited Researchers. He serves as the Deputy Editor of the Journal of Immunology and Regenerative Medicine, Section Editor for PLoS Pathogens, and Advisory Editor for the Journal of Clinical Investigation and Journal of Experimental Medicine. Dr. Wynn has organized several meetings and collaborates with the pharmaceutical industry.
Thursday, June 15
1:00 PM – 1:25 PM
Clara Abraham, MD, is an Associate Professor of Medicine at Yale University. She focuses on innate immunity and mechanisms mediating intestinal immune homeostasis, and how these mechanisms are dysregulated in diseases of intestinal inflammation, such as inflammatory bowel disease (IBD). In particular, she has utilized the insight from IBD genetic association studies to determine how the IBD genetic risk variants modulate innate immune responses and macrophage function.
Thursday, June 15
1:40 PM – 2:05 PM
University of California, San Diego
Dr. Glass received M.D. and Ph.D. degrees from UC San Diego and performed internship and residency training in Internal Medicine at Brigham and Women's Hospital. He returned to UC San Diego for fellowship training in Endocrinology and Metabolism and then joined the UC San Diego faculty. He is currently Professor of Cellular and Molecular Medicine and Professor of Medicine at UC San Diego. Dr. Glass has had a long-standing interest in elucidating the molecular mechanisms by which sequence specific transcription factors, co-activators and co-repressors regulate the development and function of macrophages in health and disease. His current studies use a combination of genetics and genomics to define molecular mechanisms specifying transcriptional regulatory elements that establish macrophage identity and cell-specific responses to environmental signals. Dr. Glass’ laboratory is currently applying these approaches to understand pathological programs of macrophage gene expression that promote the development of atherosclerosis, diabetes, cancer and neurodegenerative diseases.
Thursday, June 15
2:20 PM – 2:45 PM