Chronic schistosome infection results in the suppression of host immune responses, allowing long-term schistosome survival and restricting pathology.Current theories suggest that Treg play an important role in this re...Chronic schistosome infection results in the suppression of host immune responses, allowing long-term schistosome survival and restricting pathology.Current theories suggest that Treg play an important role in this regulation.However, the mechanism of Treg induction during schistosome infection is still unknown.The aim of this study was to determine the mechanism behind the induction of CD4(+)CD25(+) T cells by Schistosoma japonicum HSP60(SjHSP60)-derived peptide SJMHE1 as well as to elucidate the cellular and molecular basis for the induction of CD4(+)CD25(+) T cells during S.japonicum infection.Mice immunized with SJMHE1 or spleen and LN cells from naive mice pretreated.with SJMHE1 in vitro all displayed an increase in CD4(+)CD25(+) T-cell populations.Release of IL-10 and TGF-beta by SJMHE1 stimulation may contribute to suppression.Adoptively transferred SJMHE1induced CD4(+)CD25(+) T cells inhibited delayed-type hypersensitivity in BALB / c mice.Additionally, SJMHE1-treated APC were tolerogenic and induced CD4(+) cells to differentiate into suppressive CD4(+)CD25(+) Treg.Furthermore, our data support a role for TLR2 in SJMHE1-mediated CD4(+)CD25(+) Treg induction.These findings provide the basis for a more complete understanding of the S.japonicum-host interactions that contribute to host homeostatic mechanisms, preventing an excessive immune response.展开更多
文摘Chronic schistosome infection results in the suppression of host immune responses, allowing long-term schistosome survival and restricting pathology.Current theories suggest that Treg play an important role in this regulation.However, the mechanism of Treg induction during schistosome infection is still unknown.The aim of this study was to determine the mechanism behind the induction of CD4(+)CD25(+) T cells by Schistosoma japonicum HSP60(SjHSP60)-derived peptide SJMHE1 as well as to elucidate the cellular and molecular basis for the induction of CD4(+)CD25(+) T cells during S.japonicum infection.Mice immunized with SJMHE1 or spleen and LN cells from naive mice pretreated.with SJMHE1 in vitro all displayed an increase in CD4(+)CD25(+) T-cell populations.Release of IL-10 and TGF-beta by SJMHE1 stimulation may contribute to suppression.Adoptively transferred SJMHE1induced CD4(+)CD25(+) T cells inhibited delayed-type hypersensitivity in BALB / c mice.Additionally, SJMHE1-treated APC were tolerogenic and induced CD4(+) cells to differentiate into suppressive CD4(+)CD25(+) Treg.Furthermore, our data support a role for TLR2 in SJMHE1-mediated CD4(+)CD25(+) Treg induction.These findings provide the basis for a more complete understanding of the S.japonicum-host interactions that contribute to host homeostatic mechanisms, preventing an excessive immune response.
