• Modeling Mechanism：

  MOG (35-55) TFA can activate CD4⁺ T cells (Th1 and Th17 subsets), triggering CNS inflammatory infiltration, demyelination, and neurological dysfunction (T cell-mediated in WT mice); GILT⁻/⁻ mice, due to antigen processing defects, cannot process MOG protein into MOG₃₅₋₅₅ epitopes, leading to a shift in the pathogenic mechanism to antibody-mediated—producing pathogenic antibodies that recognize naturally glycosylated MOGs, which bind to MOGs on the surface of oligodendrocytes (OLs), inducing changes in cell morphology and dysfunction, while CNS infiltration is mainly in plasma cells.

• Related Products：

  MOG (35-55) TFA (TP1091)

• Modeling Method：

  Experimental Subject：

  Mice: C57BL/6 (WT), GILT⁻/⁻ (C57BL/6 background); female; 6–10 weeks old

  Dosage and Administration Route：

  300 μg MOG₃₅₋₅₅ peptide or 100 μg recombinant rat MOG protein, Emulsified in CFA containing 300 μg Mycobacterium tuberculosis, Subcutaneous injection; 500 ng pertussis toxin, Intraperitoneal injection

  Dosing Frequency and Duration Model：

  Immunisation: 1 dose each on days 0 and 7 (antigen+CFA); 1 dose each on days 0 and 2 (PTX)

• Validation：

  WT mice showed significant immunopathogenesis with MOG₃₅₋₅₅ (highest score 3.25), while GILT⁻/⁻ mice with rratMOG showed even more severe immunopathogenesis (highest score 4.25); inflammatory infiltration was observed in the CNS tissues (predominantly monocytes in WT, and predominantly CD38⁺CD138⁺ plasma cells in GILT⁻/⁻); serum anti-MOG antibody titers in GILT⁻/⁻ mice were > 1:25600, indicating the possibility of passive transfer of EAE.

*Precautions： All mice were sacrificed 40 days after modeling.

*References：Bergman CM,et,al. A switch in pathogenic mechanism in myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis in IFN-γ-inducible lysosomal thiol reductase-free mice. J Immunol. 2012 Jun 15;188(12):6001-9.