oai:pubmedcentral.nih.gov:1092...
BioMed Central
BMC Neuroscience
2024
6/11/2024
BACKGROUND: Myelin oligodendrocyte glycoprotein-associated disorders (MOGAD) is an autoimmune central nervous system disease.
Antigen-specific immune tolerance using nanoparticles such as Polylactic-co-glycolic acid (PLGA) have recently been used as a new therapeutic tolerization approach for CNS autoimmune diseases.
We examined whether MOG(1-125) conjugated with PLGA could induce MOG-specific immune tolerance in an experimental autoimmune encephalitis (EAE) mouse model.
EAE was induced in sixty C57BL/6 J wild-type mice using MOG(1-125) peptide with complete Freund’s Adjuvant.
The mice were divided into 12 groups (n = 5 each) to test the ability of MOG(1-125) conjugated PLGA intervention to mitigate the severity or improve the outcomes from EAE with and without rapamycin compared to antigen alone or PLGA alone.
EAE score and serum MOG-IgG titers were compared among the interventions.Kindly check and confirm the processed Affiliation “4” is appropriate.I confirmed the Aff 4.
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RESULTS: Mice with EAE that were injected intraperitoneally with MOG(1-125) conjugated PLGA + rapamycin complex showed dose-dependent mitigation of EAE score.
Intraperitoneal and intravenous administration resulted in similar clinical outcomes, whereas 80% of mice treated with subcutaneous injection had a recurrence of clinical score worsening after approximately 1 week.
Although there was no significant difference in EAE scores between unconjugated-PLGA and MOG-conjugated PLGA, serum MOG-IgG tended to decrease in the MOG-conjugated PLGA group compared to controls.
CONCLUSION: Intraperitoneal administration of PLGA resulted in dose-dependent and longer-lasting immune tolerance than subcutaneous administration.
The induction of immune tolerance using PLGA may represent a future therapeutic option for patients with MOGAD.
Wright, Amy E.,Nishiyama, Shuhei,Han, Patrick,Kong, Philip,Levy, Michael, 2024, Administration methods and dosage of poly(lactic acid)-glycol intervention to myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalitis mice, BioMed Central