Toxocara canis-originated recombinant C-type lectin improves the disability scores of experimental autoimmune encephalomyelitis in murine in vivo models

Abstract

Background

The recombinant C-type lectin protein (r-CTL) derived from Toxocara canis larvae is thought to play a role in promoting regulatory T cell-dominant immune responses in toxocariasis. This study aimed to highlight the therapeutic potential of the r-CTL protein in improving the disability scores of EAE by enhancing the Foxp3⁺-CD25⁺ T cells population.

Methods

The r-CTL was expressed in prokaryotic systems and purified using Ni-NTA spin columns. Balb/C57 mice were divided into six groups, with EAE induced in four of them, excluding the healthy control group and the group receiving only r-CTL treatment. 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.

Results

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.

Conclusion

In conclusion, the observed improvements in disability scores in the EAE mouse model suggest that r-CTL protein could be a potential new treatment approach worth further investigation.