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Development of Experimental Autoimmune Encephalomyelitis Critically Depends on CD 137 Ligand Signaling.
- Source :
- Journal of Neuroscience; 12/12/2012, Vol. 32 Issue 50, p18246-18252, 7p
- Publication Year :
- 2012
-
Abstract
- Multiple sclerosis (MS) is a degenerative autoimmune disease of the CNS. Experimental autoimmune encephalomyelitis (EAE) is a commonly used murine model for MS. Here we report that CD137 ligand (CD137L, 4-1BB ligand, TNFS9), a member of the TNF super-family, is critical for the development of EAE. EAE symptoms were significantly ameliorated in CD137L<superscript>-/-</superscript> mice. In the absence of CD137L, myelin oligodendrocyte glycoprotein (MOG)-specific T-cells secreted lower levels of T<subscript>h</subscript>l/T<subscript>h</subscript>17 cell-associated cytokines. MOG-specific T-cells also trafficked less efficiently to the CNS in CD 137L<superscript>-/-</superscript> mice, possibly as a consequence of reduced expression of vascular cell adhesion molecule-1 (VCAM-1), which regulates leukocyte extravasation. Thus, CD137L regulates many functions of MOG-specific T-cells that contribute to EAE and may represent a novel therapeutic target for the treatment of MS. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 02706474
- Volume :
- 32
- Issue :
- 50
- Database :
- Complementary Index
- Journal :
- Journal of Neuroscience
- Publication Type :
- Academic Journal
- Accession number :
- 84347888
- Full Text :
- https://doi.org/10.1523/JNEUROSCI.2473-12.2012