A collaborative work of scientists from the University of Würzburg and Joslin Diabetes Center has demonstrated how a genetic variant associated with type 1 diabetes and other autoimmune diseases influences susceptibility to autoimmunity.
Recent studies of the human genome have identified genetic regions associated with autoimmune diseases such as type 1 diabetes. One of these genes is PTPN22, which plays a role in lymphocyte (immune cell) function. A PTPN22 variant (or mutation) has been implicated as a risk factor for type 1 diabetes and several other autoimmune disorders.
When PTPN22 was turned off in mice, mimicking a loss-of-function mutation, the researchers observed an increase in regulatory T cells and a decreased risk of autoimmune diabetes. “This is the first study conducted on the diabetic mouse model that supports the LYP gain-of-function hypothesis,” says Dr. Kissler. “Our work should help to resolve the controversy.”
The Joslin scientists are following up on this study to deepen understanding of how inhibiting PTPN22 affects T and B cells.
The findings appear in the upcoming issue of Diabetes.
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