Myelin-reactive B cells exacerbate CD4⁺ T cell-driven CNS autoimmunity in an IL-23-dependent manner.

ABSTRACT: B cells and T cells collaborate in multiple sclerosis (MS) pathogenesis. IgH^[MOG] mice possess a B cell repertoire skewed to recognize myelin oligodendrocyte glycoprotein (MOG). Here, we show that upon immunization with the T cell-obligate autoantigen, MOG_[35-55], IgH^[MOG] mice develop rapid and exacerbated experimental autoimmune encephalomyelitis (EAE) relative to wildtype (WT) counterparts, characterized by aggregation of T and B cells in the IgH^[MOG] meninges and by CD4⁺ T helper 17 (Th17) cells in the CNS. Production of the Th17 maintenance factor IL-23 is observed from IgH^[MOG] CNS-infiltrating and meningeal B cells, and in vivo blockade of IL-23p19 attenuates disease severity in IgH^[MOG] mice. In the CNS pa

SUBMITTER: Fazazi MR 

PROVIDER: S-EPMC11208426 | biostudies-literature | 2024 Jun

REPOSITORIES: biostudies-literature