Symposium 2013: Immunity and Autoimmunity in Vasculitis

All forms of vasculitis are caused by components of the immune system damaging blood vessels. However, the way that this occurs is very different in different forms of vasculitis. Most forms of vasculitis are thought to be autoimmune, meaning that the immune system has made a response inappropriately against normal components of the human body. A few forms of vasculitis are known to be caused by immune responses to infections or to medications. Dr. Paul Monach, director of the Boston University Vasculitis Center, will provide an overview of components of the immune system, followed by descriptions of how those components work together to cause different forms of vasculitis, with emphasis on the ways in which different medications used in vasculitis interrupt these pathways to provide effective treatment.

The 2013 Vasculitis Symposium will be held at the Loews Hotel in Philadelphia, Pennsylvania, July 12-14. To learn more, click here.

The BU Vasculitis Center is a member of the Vasculitis Clinical Research Consortium (VCRC) and Dr. Monach is a co-investigator in multi-center clinical trials in multiple vasculitides. His research interests include:

1. Biomarkers in vasculitis. The long-term goal is to identify markers that are helpful for diagnosing, staging, or providing prognostic information in vasculitis. Using samples from a recent clinical trial, they have recently identified multiple cytokines, chemokines, and markers of vascular injury that are promising leads for future studies aimed at assessing clinical utility.

2.  Genetics of vasculitis. The goal is to gain insight into the pathophysiology of the vasculitides by identifying genetic variants that confer risk. Current work is focused on 192 polymorphisms previously associated with other, seemingly unrelated autoimmune diseases.

3. Neutrophils in inflammatory diseases. Investigating gene expression in mouse neutrophils as part of the Immunological Genome Project, and hopefully to translate these findings into work on neutrophil biology in human inflammatory diseases.