Lymphotoxin-α release from B cells impairs neuronal activity in coculture models, which is reversible upon BTK inhibitor treatment.

Pape et al. link the CD5-CK2-STAT3 signalling pathway to both inflammation and effector function in multiple sclerosis, using a multi-modal approach that c

A clinically available AMPAR antagonist inhibits T cell egress from lymph nodes and shows therapeutic effects in mouse models of multiple sclerosis.