2006-2007
The following is a description of a study from one of the many researchers that our organization has funded.
DRAK2: Target for New Therapy
Martina Gatzka, M.D.
University of California
Irvine, California
Modulation of central and peripheral immunological tolerance by DRAK2, a negative regulator of lymphocyte signaling
When T lymphocytes, a type of white blood cell, cannot distinguish between self and non-self tissues, they contribute to inflammation and tissue destruction in autoimmune diseases such as rheumatoid arthritis and lupus.
In healthy individuals, the immune system removes a number of natural surveillance mechanisms to prevent T cells from going awry. One such surveillance mechanism is called DRAK2 (DAP-related apoptotic kinase-2). Dr. Gatzka is studying DRAK2’s modulation of T cell activation using a mouse model of rheumatoid arthritis. Guided by the results of this research, future work may focus on targeting DRAK2 to develop new therapeutic agents for rheumatic diseases.
You may return to the list of research that we have funded.
