LAUSR

Nrg-1β1 dysregulation regulates responses in EAE. The current data propose that Nrg-1β1 can modulate both the innate and adaptive immune responses at the CNS levels, and its effects peripherally are mainly through the regulation of monocytes and their infiltration into the CNS. This, however, raises the possibility that Nrg-1β1 T cell responses the CNS lesions of EAE indirectly through modulation microglia and MDMs phenotype and IL-2 and IL-16. Nrg-1β1 treatment increases anti-inflammatory Tregs within the EAE lesions in the spinal cord. (5) In innate immune response, restoring Nrg-1β1 levels reduces monocytes in the blood and their infiltration into the CNS and consequently a decrease in the number of MDMs, while the recruitment of microglia remains unaffected. This was correlated with a reduction in the production of CSPGs and MMPs that are known mediators involved in the blood-CNS permeability in EAE and MS. Availability of Nrg-1β1 also supports a phenotype shift from pro-inflammatory M1 to neuroprotective M2 in both microglia and MDM populations. (6) Using LPC model, we have demonstrated that Nrg-1β1 treatment promotes differentiation of OPCs to mature myelinating oligodendrocytes that results in accelerated and improved remyelination of demyelinating lesions of the