Amelioration of Clinical Scores in an Experimental Autoimmune Encephalomyelitis (EAE) Model through Expansion of Regulat

The recombinant C-type lectin protein (r-CTL) derived from Toxocara canis larvae is thought to play a role in promoting regulatory T cells-dominant immune responses in toxocariasis. This study aimed to highlight the therapeutic potential of the r-CTL protein in ameliorate the disability scores of EAE by enhancing the regulatory T cells population. The recombinant C-type lectin was expressed in prokaryotic systems and purified through Ni-NTA spin columns. Balb/C57 mice were divided into six groups, with EAE induced in all groups except the healthy control group. Group I (n=10) received r-CTL treatment post EAE induction, Group II (n=10) underwent EAE induction only, Group III (n=5) received treatment with E. coli lysate proteins containing E. coli BL21 and plasmid pET32a without r-CTL after EAE induction, Group IV (n=5) received sterile PBS after EAE induction, Group V (n=5) served as the healthy control group, and Group VI (n=5) received only r-CTL treatment. The study's findings revealed that r-CTL treatment significantly decreased disability scores in EAE-induced mice. There was a notable increase in the population of CD4+, CD25+, FOXP3+ regulatory T cells following r-CTL treatment. The gene expression levels of IL-10, FOXP3, and GATA3 were significantly elevated in the r-CTL treated group, while the expression of T-bet and RORγ genes was reduced. Treatment with r-CTL significantly mitigated cell infiltration and demyelination in both the spinal cord and brain. In conclusion, these findings suggest that the r-CTL protein may have promising applications in the treatment of MS and warrant further investigation into its therapeutic mechanisms.