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Death-resistant T cells in female mice with lupus
Proper defense of the body against germs requires the actions of specialized cells of the immune system, known as T cells. Activated T cells must eventually be silenced, or autoimmune diseases such as lupus can result. Researcher Alessandra Pernis and colleagues at Columbia University in New York now show that genetically modified mice that do not express a T cell protein called IBP (IFN regulatory factor-4binding protein) develop spontaneous autoimmunity and lupus-like disease. The study, which appears online on February 9 in advance of print publication in the March issue of the Journal of Clinical Investigation, found that most of these affected IBP "knockout" mice were females, similar to the higher incidence of lupus in females than males in humans. The researchers noticed that unlike their normal siblings, 60% of the female IBP knockout mice developed enlarged lymph nodes, easily observed as swollen lumps in their necks at 5 months of age. Further analysis revealed that these IBP knockout T cells were resistant to death and failed to produce enough of a critical immune protein called IL-2 (interleukin-2). These animals provide an important model to understand lupus and other autoimmune disorders, and the authors suggest that investigating IBP in human autoimmunity warrants consideration.
TITLE: Loss of IRF-4binding protein leads to the spontaneous development of systemic autoimmunity
Alessandra B. Pernis
Columbia University, New York, New York, USA
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