Schistosoma japonicum HSP60-derived peptide SJMHE1 suppresses delayed-type hypersensitivity in a murine model

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. © 2016 wang et al.