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• W4386817668 abstract "Abstract Toxocara canis is a global zoonosis infection that can cause chronic and long‐term toxocariasis in their paratenic host. The excretory‐secretory (ES) products of T . canis larvae are considered to be responsible for the Th2 polarization and regulatory immune responses in toxocariasis. The C‐type lectin family is one of the most prominent components of ES products of T . canis infective larvae. This study aimed to investigate the ameliorative effect of a T . canis C‐type lectin recombinant protein (rCTL), on experimental autoimmune encephalomyelitis (EAE) which is a T‐cell‐mediated autoimmune disease of the central nervous system. C57BL/6 mice were subcutaneously treated with 30 μg rCTL, three times at an interval of 1 week. EAE was induced by myelin oligodendrocyte glycoprotein 35–55 peptide (MOG35‐55 peptide) immunization, and weight and clinical scores were evaluated. Real time polymerase chain reaction was performed to evaluate the expression levels of T ‐ bet , Gata3 , and Foxp3 in splenocytes. In addition, the levels of interleukin 4, interferon gamma, and tumour growth factor‐β (TGF‐β) were quantified by enzyme‐linked immunosorbent assay in splenocyte culture supernatants. The results indicated that the rCTL decreased clinical disability scores and delayed the onset of EAE. Furthermore, the data showed that rCTL treatment modulated the immune response, which was associated with upregulation of the mRNA expression of the Foxp3 gene and higher production of TGF‐β in rCTL‐treated mice. This study demonstrated that rCTL might be a potential agent to ameliorate EAE symptoms by stimulating anti‐inflammatory responses." @default.
• W4386817668 created "2023-09-19" @default.
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• W4386817668 date "2023-09-18" @default.
• W4386817668 modified "2023-10-16" @default.
• W4386817668 title "The immunomodulatory effects of the <scp>C‐</scp>type lectin protein of <i>Toxocara canis</i> on experimental autoimmune encephalomyelitis" @default.
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• W4386817668 doi "https://doi.org/10.1111/pim.13010" @default.
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