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Immunology. 2011 Jul;133(3):370-8. doi: 10.1111/j.1365-2567.2011.03450.x. Epub 2011 May 13.

Neuroprotective role of fibroblast growth factor-2 in experimental autoimmune encephalomyelitis.

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  • 1Department of Anatomy I, University of Cologne, Germany.


The role of fibroblast growth factor-2 (FGF-2) in multiple sclerosis and its animal model experimental autoimmune encephalomyelitis is discussed. This study is the first to use FGF-2(-/-) mice to further address the involvement of FGF-2 in the disease process. We demonstrate that immunization with myelin oligodendrocyte glycoprotein peptide 35-55 induces more severe experimental autoimmune encephalomyelitis in FGF-2(-/-) mice compared with FGF-2(+/+) mice. The antigen-specific cytokine response to myelin oligodendrocyte glycoprotein peptide and the degree of central nervous system inflammation was similar in both groups. However, FGF-2(-/-) mice displayed increased infiltration of CD8(+) T cells and macrophages/microglia. In addition, nerve fibre degeneration and axonal loss were augmented, whereas the extent of remyelination in central nervous system lesions was reduced. FGF-2 has been associated with the induction of demyelination and the inhibition of myelin production by oligodendrocytes. Our study supports the opposing notion that FGF-2 can also assert a neuroprotective function. This may be particularly appealing when it comes to targeting the neurodegenerative aspect of multiple sclerosis.

© 2011 The Authors. Immunology © 2011 Blackwell Publishing Ltd.

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