Nogo-receptor 1 expression on B-cell populations in the central nervous system during experimental autoimmune encephalomyelitis

International Congress on Neuroimmunology and Therapeutics

DoubleTree by Hilton Hotel San Francisco Airport, San Francisco, CA, USA

Maha Bakhuraysah, Amani Alrehaili, Jae Young Lee, Peimun Aui and Steven Petratos

Posters-Accepted Abstracts: J Neurol Disord

Abstract :

Although the fact that deletion of Nogo receptor 1 (NgR1) can protect against axonal degeneration and thus progression of disease, in the animal model of multiple sclerosis (MS), experimental autoimmune encephalomyelitis (EAE), the immunological role of this receptor is unclear. To further understand the function of NgR1 in regulating immune cells, flow cytometry-based phenotypic analysis was performed on isolates from spleens, lymph nodes and spinal cords at different clinically defined stages of EAE disease. The central nervous system (CNS)-infiltrating blood cells revealed an augmented response in the B-cell population, which expressed NgR, seeing in ngr1+/+ mice with the onset and progression of the disease. This population of cells could not be demonstrated within the spinal cords of EAE-induced ngr1-/- mice or during the chronic stage of disease in ngr1+/+ mice. At the onset of disease onset, there was a significant increase in IgM-B-cells-expressing NgR in the spinal cord, when compared with the IgD populations. Remarkably, there was a cluster of B-cells expressing NgR present at the meninges of the spinal cords of ngr1+/+ EAE-induced mice at clinical score 1.5 and these cells localised within small follicles in submeningeal regions. Furthermore, there was clustering of B-cell activating factor (BAFF) and NgR-positive immune cell infiltrates within the spinal cords of EAE-induced ngr1+/+ mice at disease onset. Collectively, these data indicate that there exists the inducible expression of NgR1 in specific immune lineage cells upon the induction of EAE, as well as, a strong correlation between the expression profiles of NgR1 and BAFF on neighbouring B-cells within spinal cord follicular structures.