sp1 inhibitor plicamycin  (MedChemExpress)

Journal: Communications Biology

Article Title: Decidual natural killer cells dysfunction is caused by IDO downregulation in dMDSCs with Toxoplasma gondii infection

doi: 10.1038/s42003-024-06365-5

Figure Lengend Snippet: a The AhR and SP1 expressions in human dNK cells in the co-culture system were detected by western blot (data represent the mean ± SD from three independent experiments by paired t -test). b In the co-culture system, AhR and SP1 in human dNK cells were detected by western blot in infected group, 1-MT-treated infected group and Kyn-treated infected group (data represent the mean ± SD from three independent experiments by one-way ANOVA). c The AhR expressions in mouse dNK cells were analyzed by flow cytometry in uninfected ( n = 9), infected ( n = 10) and IDO –/– infected pregnant mice ( n = 8). d The AhR expressions in mouse dNK cells were detected by flow cytometry in infected, IDO –/– infected and Kyn-treated IDO –/– infected pregnant mice ( n = 6). The expressions of AhR, SP1, TGF-β and IL-10 in human dNK cells of the co-culture system were examined by western blot after treated with AhR inhibitor CH-223191 ( e ) or SP1 inhibitor Plicamycin ( f ), respectively (data represent the mean ± SD from three independent experiments by one-way ANOVA). Mice samples in each group assayed individually by one-way ANOVA. * P < 0.05, ** P < 0.01, MFI: mean fluorescence intensity.

Article Snippet: To investigate the role of the Kyn/AhR/SP1 pathway, the co-cultured cells were divided into five groups: infected, IDO inhibitor (1-methyl-tryptophan, 1-MT; Sigma-Aldrich, UK)-treated infected, exogenous kynurenine (Kyn; MCE, China)-treated infected, AhR inhibitor (CH-223191; MCE, China)-treated infected, and SP1 inhibitor (Plicamycin; MCE, China)-treated infected groups.

Techniques: Co-Culture Assay, Western Blot, Infection, Flow Cytometry, Fluorescence

Journal: Communications Biology

Article Title: Decidual natural killer cells dysfunction is caused by IDO downregulation in dMDSCs with Toxoplasma gondii infection

doi: 10.1038/s42003-024-06365-5

Figure Lengend Snippet: T. gondii infection upregulated the transcriptional levels of IDO in dMDSCs through STAT3/p52-RelB pathway. But IDO protein expression was decreased due to the degradation induced by the increase of SOCS3 by infection, which in turn the reduction of IDO metabolite kynurenine further downregulated TGF-β and IL-10 expression in dNK cells through Kyn/AhR/SP1 signaling pathway, ultimately leading to the dysfunction of dNK and the disorders of maternal-fetal tolerance.

Article Snippet: To investigate the role of the Kyn/AhR/SP1 pathway, the co-cultured cells were divided into five groups: infected, IDO inhibitor (1-methyl-tryptophan, 1-MT; Sigma-Aldrich, UK)-treated infected, exogenous kynurenine (Kyn; MCE, China)-treated infected, AhR inhibitor (CH-223191; MCE, China)-treated infected, and SP1 inhibitor (Plicamycin; MCE, China)-treated infected groups.

Techniques: Infection, Expressing