Treatment of spontaneous EAE by laquinimod reduces Tfh, B cell aggregates, and disease progression.

ABSTRACT:

Objective

To evaluate the influence of oral laquinimod, a candidate multiple sclerosis (MS) treatment, on induction of T follicular helper cells, development of meningeal B cell aggregates, and clinical disease in a spontaneous B cell-dependent MS model.

Methods

Experimental autoimmune encephalomyelitis (EAE) was induced in C57BL/6 mice by immunization with recombinant myelin oligodendrocyte glycoprotein (rMOG) protein. Spontaneous EAE was evaluated in C57BL/6 MOG p35-55-specific T cell receptor transgenic (2D2) × MOG-specific immunoglobulin (Ig)H-chain knock-in (IgH^MOG-ki [Th]) mice. Laquinimod was administered orally. T cell and B cell populations were examined by flow cytometry and immunohistochemistry.

Results

Oral laquinimod treatment (1) reduced CD11c

SUBMITTER: Varrin-Doyer M 

PROVIDER: S-EPMC5032667 | biostudies-literature | 2016 Oct

REPOSITORIES: biostudies-literature