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Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues
Published on: May 8, 2016
Aggravated experimental autoimmune encephalomyelitis in IL-15 knockout mice
Diego Gomez-Nicola1, Alessandra Spagnolo, Carmen Guaza
1Neural Plasticity Group, Functional and Systems Neurobiology Department, Instituto Cajal, Consejo Superior de Investigaciones Científicas, 28002 Madrid, Spain.
Experimental Neurology
|January 15, 2010
Summary
Interleukin-15 (IL-15) absence worsens experimental autoimmune encephalomyelitis (EAE), a multiple sclerosis model, by increasing inflammation and demyelination. This suggests IL-15 plays a protective role in this autoimmune disease.
Area of Science:
- Immunology
- Neuroscience
- Autoimmune Diseases
Background:
- Interleukin-15 (IL-15) shares similarities with IL-2 and is linked to autoimmune diseases.
- Information on IL-15's role in multiple sclerosis (MS) pathogenesis is limited.
Purpose of the Study:
- To investigate the impact of IL-15 absence on experimental autoimmune encephalomyelitis (EAE), a mouse model for MS.
- To understand the role of IL-15 in the development and severity of EAE.
Main Methods:
- Comparison of EAE development in IL-15 knockout (IL-15(-/-)) mice and wild-type (C57BL/6) mice.
- Immunization with MOG(35-55) to induce EAE.
- Assessment of neurological impairment, demyelination, immune cell infiltration, and inflammation in the spinal cord.
Main Results:
- IL-15(-/-) mice exhibited more severe neurological impairment compared to wild-type mice.
- Greater demyelination, increased immune cell infiltration, and heightened inflammation were observed in IL-15(-/-) mice.
- IL-15(-/-) mice showed a higher CD4/CD8 ratio, reduced NK cell activity, and overexpression of CX3CR1 on CD8(+) T cells.
Conclusions:
- The absence of IL-15 exacerbates EAE severity, suggesting a potentially protective role for IL-15 in MS pathogenesis.
- The observed immune alterations (CD4/CD8 ratio, NK cell activity, CX3CR1 expression) in IL-15(-/-) mice may contribute to aggravated EAE.
- Further investigation is required to elucidate the precise mechanisms by which these findings contribute to EAE development.
