Aggravated experimental autoimmune encephalomyelitis in IL-15 knockout mice
Gomez-Nicola, Diego, Spagnolo, Alessandra, Guaza, Carmen and Nieto-Sampedro, Manuel (2010) Aggravated experimental autoimmune encephalomyelitis in IL-15 knockout mice. Experimental Neurology, 222, (2), 235-242. (doi:10.1016/j.expneurol.2009.12.034). (PMID:20070942).
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IL-15 initially identified as a T proliferating cytokine has several structural and biological similarities with IL-2 and has been associated with a number of autoimmune diseases. Because of the scarcity of information available on the role of IL-15 in MS pathogenesis, we have investigated how the absence of IL-15 affected the development of experimental autoimmune encephalomyelitis, a mouse model of MS. Following immunization of IL-15(-/-) and C57BL/6 mice with MOG(35-55), we observed a more severe neurological impairment in the IL-15 knockout mice than in the wild-type group. The enhanced disease severity in IL-15(-/-) mice was associated with greater demyelination in the spinal cord, increased immune cell infiltration and inflammation. These events may be related to the higher CD4/CD8 ratio and the almost absent NK cell activity, congenital immune features of IL-15KO mice. Moreover, we found that the fractalkine receptor CX3CR1 was overexpressed in the spinal cord of IL-15(-/-) mice, mainly localized on infiltrating CD8(+) T cells. How these findings are contributing to the aggravated EAE development in IL-15 KO mice remain unclear and need to be further investigated.
|Digital Object Identifier (DOI):||doi:10.1016/j.expneurol.2009.12.034|
|Keywords:||CD4, CD8, CX3CR1, multiple sclerosis, cytokines, demyelination|
|Subjects:||Q Science > QR Microbiology > QR180 Immunology
R Medicine > RC Internal medicine > RC0321 Neuroscience. Biological psychiatry. Neuropsychiatry
|Divisions:||Faculty of Natural and Environmental Sciences > Biological Sciences > Biomedicine
|Date Deposited:||02 Mar 2012 16:58|
|Last Modified:||27 Mar 2014 20:19|
|RDF:||RDF+N-Triples, RDF+N3, RDF+XML, Browse.|
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