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Blockade of fat hormone helps halt and heal multiple sclerosis

JCI Journals

Italian researchers have found that blockade of the hormone leptin, which is primarily produced in fats cells, has beneficial effects on the induction and progression of experimental autoimmune encephalomyelitis (EAE) in mice - the animal model of human multiple sclerosis (MS). In their study appearing online on January 12 in advance of print publication in the February 2006 issue of the Journal of Clinical Investigation, Giuseppe Matarese and colleagues from Università di Napoli "Federico II" suggest that leptin neutralization may be a potential way to both prevent and treat MS.

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

Giuseppe Matarese
Università di Napoli "Federico II", Napoli, Italy.
Phone: 39-081-7463311
Fax: 39-081-7463252

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