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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.

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