TCDD attenuates EAE through induction of FasL on B cells and inhibition of IgG production.

ABSTRACT: Previously we demonstrated that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) suppressed experimental autoimmune encephalomyelitis (EAE), a model to study multiple sclerosis (MS), through induction of regulatory T cells (Tregs) and suppression of effector T cell function in the spleen. Since B cells and specifically regulatory B cells (Bregs) have been shown to be so critical in the pathology associated with EAE and MS, we wanted to determine whether TCDD could also induce Bregs. We specifically hypothesized that a Fas ligand (FasL)+ Breg population would be induced by TCDD in EAE thereby triggering apoptosis in Fas-expressing effector T cells as one mechanism to account for inhibition of T cell function by TCDD. TCDD (0.1-2.5 μg/kg/day administered orally for 12 days) modestly increased the

SUBMITTER: Kummari E 

PROVIDER: S-EPMC7785643 | biostudies-literature | 2021 Jan

REPOSITORIES: biostudies-literature