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New research published today in eLife demonstrates a new function for Wiskott-Aldrich Syndrome (WAS) protein in the activation of T cells, which play a central role in our immune system.

New research published today in eLife demonstrates a new function for Wiskott-Aldrich Syndrome (WAS) protein in the activation of T cells, which play a central role in our immune system.

The study, led by Professor Michael Dustin of the Kennedy Institute, NDORMS in collaboration with Dr Sudha Kumari at MIT furthers our understanding of the regulation of T cell activation – an essential part of our immune response to different types of diseases – and its dysfunction in WAS patients.

WAS is a rare serious disease affecting between 1 and 10 people in a million worldwide, usually male (90%). People suffering from WAS have abnormal or nonfunctional white blood cells (which are part of the immune system) and are at increased risk of developing several immune and inflammatory disorders. There is also a significant reduction in the size and number of platelets, causing those affected to bleed easily.

The condition is caused by mutations or defects in the WAS gene, responsible for giving the instruction to make the Wiskott-Aldrich Syndrome Protein (WASP).  WASP is known to be able to produce new actin cytoskeleton, a network of fibers that make up the cell's structural framework.  The new research identifies how WASP is involved in passing on signals from the surface of T cells through the actin cytoskeleton to the cells core.

Professor Dustin says: “This was a heroic effort by Dr. Kumari, which required an arsenal of new tools. This effort opens a way forward to much needed new therapeutics for WAS and more common immunological diseases such as allergies.”

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