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.
Flow Cytometric Analysis of Lymphocyte Infiltration in Central Nervous System during Experimental Autoimmune Encephalomyelitis
Adjuvant Activity of Mycobacterium paratuberculosis in Enhancing the Immunogenicity of Autoantigens During Experimental Autoimmune Encephalomyelitis
Induction and Diverse Assessment Indicators of Experimental Autoimmune Encephalomyelitis
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