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), pp. 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.

Item Type: Article
Digital Object Identifier (DOI): doi:10.1016/j.expneurol.2009.12.034
ISSNs: 0014-4886 (print)
Keywords: CD4, CD8, CX3CR1, multiple sclerosis, cytokines, demyelination
Organisations: Biomedicine
ePrint ID: 333258
Date :
Date Event
January 2010e-pub ahead of print
April 2010Published
Date Deposited: 02 Mar 2012 16:58
Last Modified: 17 Apr 2017 17:29
Further Information:Google Scholar

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