Generation of Experimental Autoimmune Encephalomyelitis in a Mouse Model

Inject the myelin-derived peptides with an adjuvant near the peripheral lymph nodes of an anesthetized mouse.

The peptide-adjuvant conjugates activate the antigen-presenting cells, or APCs, which recognize and process the peptides.

The APCs then migrate to the lymph nodes and activate the autoreactive T cells.

Periodically inject the pertussis toxin intraperitoneally, which disrupts the tight junctions between the endothelial cells and increases the blood-brain barrier permeability.

The autoreactive T cells circulate in the blood and cross the blood-brain barrier to enter the brain tissue.

These cells recognize the peptides on the myelin sheath and release the cytokines.

These cytokines recruit macrophages and B cells to the site.

Macrophages release reactive oxygen species that damage the myelin-producing oligodendrocytes, while the B cells interact with T cells, become activated, and produce autoantibodies targeting the myelin sheath.

This leads to demyelination, impairing nerve transmission.

Lift the mouse tail; a gradual drop indicates nerve damage, signaling the onset of autoimmune encephalomyelitis, or EAE.

Begin this procedure with anesthetization of C57BL/6 mice that have b