1. Schistosoma japonicum HSP60-derived peptide SJMHE1 suppresses delayed-type hypersensitivity in a murine model.
- Author
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Xuefeng Wang, Jun Wang, Yong Liang, Hongchang Ni, Liang Shi, Chengcheng Xu, Yuepeng Zhou, Yuting Su, Xiao Mou, Deyu Chen, and Chaoming Mao
- Subjects
SCHISTOSOMA japonicum ,PEPTIDES ,PARASITES ,T cells ,MICE - Abstract
Background: Parasite-derived molecules with immunomodulatory properties, which have been optimised during host-parasite co-evolution, exhibit potential applications as novel immunotherapeutics. We have previously demonstrated that Schistosoma japonicum HSP60-derived peptide SJMHE1 induces CD4
+ CD25+ regulatory T-cells (Tregs) and that adoptively transferred SJMHE1-induced CD4+ CD25+ Tregs inhibit delayed-type hypersensitivity (DTH) in mice. However, multiple concerns regarding this method render this treatment unsuitable. To gain further insights into the potential effects of SJMHE1, we used ovalbumin (OVA)-induced DTH and evaluated the effect of SJMHE1 on DTH mice. Methods: BALB/c mice were sensitised with OVA alone or combined with SJMHE1 and then challenged with OVA to induce DTH. We first analysed the potential effects of SJMHE1 by measuring DTH responses, T-cell responses, cytokine secretion, and Treg proportions. We then evaluated the expression levels of IL-10 and TGF-β1 in CD4+ CD25+ T-cells during DTH and Treg generation to identify the mechanism by which SJMHE1 suppresses DTH. Results: SJMHE1 modulated the effector response against OVA-induced DTH and stimulated the production of the anti-inflammatory cytokines IL-10 and TGF-β1 in immunised mice through a mechanism involving CD4+ CD25+ Tregs. SJMHE1-induced CD4+ CD25+ Tregs expressed high levels of CTLA-4, IL-10, and TGF-β1, which substantially contributed to the suppressive activity during DTH. The administration of SJMHE1 to DTH in mice led to the expansion of CD4+ CD25+ Tregs from CD4+ CD25- T-cells in the periphery, which inhibited DTH responses. Conclusions: Our study proves that the parasite-driven peptide suppresses DTH in mice, which may confer a new option for inflammation treatment. [ABSTRACT FROM AUTHOR]- Published
- 2016
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