MS is an inflammatory disease of the brain and spinal chord characterized by muscle weakness, numbness, and loss of coordination. These symptoms result in part from destruction of the nerve-insulating material myelin by activated T cells.
Leptin is known to play a critical role in the regulation of food intake, metabolism, and the immune response. Since it had been previously shown that leptin is expressed in active inflammatory lesions of the central nervous system during EAE and MS, Matarese and colleagues investigated the effects of leptin blockade on the induction and progression of EAE in mice. They found that leptin blockade by the use of either anti-leptin antibodies or a form of the leptin receptor unable to bind leptin, either before or after disease onset improved clinical symptoms of disease, slowed disease progression, reduced disease relapses, and reduced the number of antigen-specific T cells. The authors delved further to unravel the cellular signaling events underlying these beneficial effects. Taken together, the data provide a basis for the development and testing of novel strategies of leptin-based targeting for the potential treatment of MS.
TITLE: Leptin neutralization interferes with pathogenic T cell autoreactivity in autoimmune encephalomyelitis
Università di Napoli "Federico II", Napoli, Italy.
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