Aggravated experimental autoimmune encephalomyelitis in IL-15 knockout mice

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 scat-city 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 maybe 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 (C) 2010 Elsevier Inc All rights reserved