The Fu laboratory studies the role that autoimmunity plays an in systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). The emphasis of the Fu laboratory is on the genetic and environmental factors important for these disorders.
The hypothesis that molecular mimicry initiates the initial autoimmune response, which diversifies to multiple autoantigens, resulting in end organ damage in suitable hosts is being tested. The role of MHC in this process in both mice and humans is being investigated. In this regard, bacterial and viral agents sharing cross reactive T and B cell epitopes with human autoantigens are logical candidates for molecular mimics in this process.
Part of The Investigator's Annexe program.