Marc Charabati

TL;DR: It is shown that IgA+ PB and/or PC mobilized from the gut play an unexpected role in suppressing neuroinflammation and are dramatically reduced in the gut during EAE, and likewise, a reduction in IgA-bound fecal bacteria is seen in MS patients during disease relapse.

TL;DR: It is demonstrated that ALCAM knockout mice develop a more severe experimental autoimmune encephalomyelitis, the mouse model of MS, due to an increased permeability of the blood–brain barrier (BBB), suggesting that in addition to its role in leukocyte transmigration, A LCAM regulates and maintains tight junction stability by acting as an adaptor molecule.

TL;DR: It is proposed that melanoma cell adhesion molecule (MCAM) is a surface marker and adhesion molecules used by pathogenic CD8+ T lymphocytes to access the CNS.

TL;DR: This work reports that two microRNAs, miR-223-3p and miR -3p, are upregulated in neurons in the experimental autoimmune encephalomyelitis mouse model of CNS inflammation and in grey matter-containing multiple sclerosis lesions, and suggests that antagonism of NMDA and AMPA type glutamate receptors protects neurons from condition media dependent degeneration.

TL;DR: The findings indicate that restricting access to the CNS by targeting ALCAM on pathogenic B lymphocytes might represent a promising strategy for the development of next-generation B lymphocyte–targeting therapies for the treatment of MS.