Human regulatory T cells viewed using fluorescence microscopy after immunostaining (left). FOXP3 protein stained by anti-FOXP3 antibody within one regulatory T cell (right).
Image Credit: Kathryn T. Iacono, University of Pennsylvania School of Medicine; Proceedings of the National Academy of Sciences.
Source: University of Pennsylvania School of Medicine
(PHILADELPHIA) – Multiple sclerosis, diabetes, and arthritis are among a variety of autoimmune diseases that are aggravated when one type of white blood cell, called the immune regulatory cell, malfunctions. In humans, one cause of this malfunction is when a mutation in a gene called FOXP3 disables the immune cells’ ability to function. In a new study published online next week in the Proceedings of the National Academy of Sciences, researchers at the University of Pennsylvania School of Medicine have discovered how to modify enzymes that act on the FOXP3 protein, in turn making the regulatory immune cells work better. These findings have important implications for treating autoimmune-related diseases.
We have uncovered a mechanism by which drugs could be developed to stabilize immune regulatory cells in order to fight autoimmune diseases,” says senior author Mark Greene, MD, PhD, the John Eckman Professor of Pathology and Laboratory Medicine. “There’s been little understanding about how the FOXP3 protein actually works.” First author Bin Li, PhD, a research associate in the Greene lab has been working on elucidating this process since FOXP3’s discovery almost five years ago. [Read the full article]
No comments:
Post a Comment