Induction of Experimental Autoimmune Encephalomyelitis in a Mouse Model

Take an adjuvant emulsion containing myelin oligodendrocyte glycoproteins, or MOGs — a nerve myelin sheath protein, and inactivated Mycobacterium tuberculosis. Inject it subcutaneously into the mouse's back.

Next, intraperitoneally inject bacteria-derived exotoxins  — disturbing the blood-brain barrier.

The subcutaneously injected Mycobacterium mimics local infection, attracting immune cells, including antigen-presenting cells or APCs.

APCs interact with MOGs, processing and presenting them on the major histocompatibility complexes, MHCs.

Activated APCs migrate to the lymph nodes, where T cells interact with APCs, becoming autoreactive T cells.

These T cells enter the bloodstream, cross the barrier, and infiltrate the central nervous system, CNS.

In the CNS, autoreactive T cells interact with MOG-expressing cells, promoting immune cell infiltration.

Infiltrated monocytes differentiate into macrophages, releasing inflammatory cytokines and reactive oxygen species, causing myelin-producing oligodendrocytes' cell death.

B cells interact with autoreactive T cells, differentiating into plasma cells and secreting autoantibodies against MOG, leading to myelin sheath degradation.

The demyelination impairs nerve signal transmission, inducing autoimmune encephalomyelitis.

Begin by subcutaneously injecting 10- to 13-week-old female mice with 200 micrograms of myelin oligodendrocyte glycoprotein, emulsified in 200 microliters of complete Freund's adjuvant containing 400 micrograms of Mycobacterium tuberculosis. Immediately, and 24 hours later, intraperitoneally inject the mice with 0.2 micrograms of pertussis toxin in 200 microliters of PBS.

It is essential that mice have been adapted both to handling and the experimental environment before induction to avoid inducing stress, which can prevent the development of clinical symptoms.

One week after the injection, examine the mice daily for clinical symptoms as described in the table.