Alterations in the activity of the Deaf1 protein may influence the onset of type 1 diabetes according to a study published online in Nature Immunology. Diabetes is an autoimmune disorder induced by T cells that attack and destroy insulin-producing pancreatic beta-cells. Normally, T cells are made tolerant towards these pancreatic cells by exposure to self proteins.
C. Garrison Fathman and colleagues show that in mice Deaf1 facilitates the expression of these self proteins in pancreatic lymph nodes. However, they found that the expression of a non-functional form of Deaf1 coincides with the onset of type 1 diabetes.
Importantly, a similar non-functional form of Deaf1 is expressed in higher concentrations in type 1 diabetes patients than in healthy patients. Additional work is needed to determine if the loss of Deaf1 activity directly contributes to type 1diabetes onset, and if it is possible to therapeutically prevent expression of non-functional Deaf1 variants.
C. Garrison Fathman (Stanford University, CA, USA)
Abstract available online.
(C) Nature Immunology.
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