Induction of Experimental Autoimmune Encephalomyelitis in a Mouse Model
筆記録
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.
