论文部分内容阅读
Objective:To observe the discrepancies of responses induced by Schistosoma japonicum(S.japonicum)normal cercaria antigen(NCA)and ultraviolet(UV)-radiation-attenuated cercaria antigen(UVACA)in an in vitro system.Methods:S.japonicum cercariae were collected and UVACA and NCA were prepared.Mouse macro- phage model cells(RAW 264.7)were treated with medium,NCA(40μg/mL)or UVACA(40μg/mL)in the presence or absence of recombinant mouse interferon gamma(rmIFN-γ;4 ng/mL)for 48 h.Cell surface staining and flow cytometry were used to assess the major histocompatibility complex(MHC)Ⅱexpression,and data were expressed as mean fluorescence intensities(MFI).Interleukin(IL)-10,IL-6 and prostaglandin E2(PGE 2 ) in cell culture supernatant were evaluated by commercial enzyme-linked immunosorbent assays.Results:NCA significantly suppressed IFN-γ-induced MHCⅡexpression on RAW 264.7 cells.In the presence of IFN-γ,NCA significantly promoted IL-6,IL-10 and PGE 2 secretion from RAW 264.7 cells.In the presence of IFN-γ,UVACA significantly promoted IL-10 but not IL-6 and PGE 2 secretion from RAW 264.7 cells and showed no effect on IFN-γ-induced MHCⅡexpression.Compared with UVACA,NCA significantly suppressed IFN-γ-induced MHC Ⅱexpression and significantly promoted IL-6,PGE 2 and IL-10 secretion from RAW 264.7 cells.Conclusion: RAW 264.7 cells respond differently to NCA and UVACA.NCA can significantly suppress IFN-γ-induced MHC Ⅱexpression and significantly promote IL-6,IL-10 and PGE 2 secretion from RAW 264.7 cells compared with UVACA.
Objective: To observe the discrepancies of responses induced by Schistosoma japonicum (S. japonicum) normal cercaria antigen (NCA) and ultraviolet (UV) -radiation-attenuated cercaria antigen (UVACA) in an in vitro system. Methods: S. japonicum cercariae were collected and UVACA and NCA were prepared.Mouse macro-phage model cells (RAW 264.7) were treated with medium, NCA (40 μg / mL) or UVACA (40 μg / mL) in the presence or absence of recombinant mouse interferon gamma ; 4 ng / mL for 48 h. Cell surface staining and flow cytometry were used to assess the major histocompatibility complex (MHC) II expression, and data were expressed as mean fluorescence intensities (MFI). Interleukin (IL) -10, IL- 6 and prostaglandin E2 (PGE2) in cell culture supernatant were evaluated by commercial enzyme-linked immunosorbent assays. Results: NCA was significantly suppressed IFN- [gamma] -induced MHC II expression on RAW 264.7 cells. -6, IL-10 and PGE2 secretion from RAW 264.7 cells. In the p resence of IFN-γ, UVACA promoted IL-10 but not IL-6 and PGE 2 secretion from RAW 264.7 cells and showed no effect on IFN-γ-induced MHCⅡexpression. Compared with UVACA, NCA suppressed IFN-γ-induced MHC II expression and promoted secretion of IL-6, PGE 2 and IL-10 secretion from RAW 264.7 cells. Confocal: RAW 264.7 cells responding differently to NCA and UVACA. NCA can inhibit suppressor IFN-γ-induced MHC II expression and significantly promote IL- IL-10 and PGE 2 secretion from RAW 264.7 cells compared with UVACA.