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

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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.

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