Journal
ANNALS OF NEUROLOGY
Volume 77, Issue 5, Pages 902-908Publisher
WILEY
DOI: 10.1002/ana.24387
Keywords
-
Categories
Funding
- Deutsche Forschungsgemeinschaft [Le 3079/1-1]
- US National Multiple Sclerosis Society (NMSS) [FG 2067-A-1]
- National Health and Medical Research Council of Australia/CIRM [APP1053621]
- Victoria/CIRM Joint Project [RMI-01739]
- Department of Industry, Commonwealth of Australia [AISRF06680]
- NIH [RO1 AI073737, RO1 NS063008]
- NMSS [RG 4124]
- Guthy Jackson Charitable Foundation
- Maisin Foundation
- Biogen Idec
- Teva Pharmaceuticals
Ask authors/readers for more resources
Natalizumab, which binds very late antigen-4 (VLA-4), is a potent therapy for multiple sclerosis (MS). Studies have focused primarily upon its capacity to interfere with T-cell migration into the central nervous system (CNS). B cells are important in MS pathogenesis and express high levels of VLA-4. Here, we report that the selective inhibition of VLA-4 expression on B cells impedes CNS accumulation of B cells, and recruitment of Th17 cells and macrophages, and reduces susceptibility to experimental autoimmune encephalomyelitis. These results underscore the importance of B-cell VLA-4 expression in the pathogenesis of CNS autoimmunity and provide insight regarding mechanisms that may contribute to the benefit of natalizumab in MS, as well as candidate therapeutics that selectively target B cells. Ann Neurol 2015;77:902-908
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available