| First Author | Gomez-Nicola D | Year | 2010 |
| Journal | Exp Neurol | Volume | 222 |
| Issue | 2 | Pages | 235-42 |
| PubMed ID | 20070942 | Mgi Jnum | J:158836 |
| Mgi Id | MGI:4440701 | Doi | 10.1016/j.expneurol.2009.12.034 |
| Citation | Gomez-Nicola D, et al. (2010) Aggravated experimental autoimmune encephalomyelitis in IL-15 knockout mice. Exp Neurol 222(2):235-42 |
| abstractText | 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. |
