Induction of Experimental Autoimmune Encephalomyelitis in a Mouse Model

Begin by subcutaneously injecting an emulsion containing a neuronal peptide and a heat-killed bacterial adjuvant into an anesthetized mouse.

In the subcutaneous tissue, the adjuvant attracts antigen-presenting cells, or APCs, which process and present the neuronal peptides on major histocompatibility complexes.

The activated APCs reach the lymph nodes and interact with naïve T cells, inducing their differentiation into autoreactive T cells.

These T cells circulate and reach the blood-brain barrier or BBB.

Next, intraperitoneally inject bacteria-derived exotoxins.

The exotoxins reach the BBB, increasing its permeability and allowing T cell infiltration into the central nervous system (CNS).

In the CNS, T cells interact with resident APCs presenting the neuronal peptide, promoting cytokine release that induces further immune cell infiltration.

The immune cells release pro-inflammatory cytokines, causing myelin damage.

Additionally, B-cells interact with T cells and secrete autoantibodies that further damage myelin, establishing experimental autoimmune encephalomyelitis (EAE).

In this procedure, dissolve PTX at 2 micrograms per milliliter in 1x PBS, and mix well. Then, inject 100 micr