Journal: International journal of molecular sciences

Article Title: ULBP2 Promotes Tumor Progression by Suppressing NKG2D-Mediated Anti-Tumor Immunity.

doi: 10.3390/ijms26072950

Figure Lengend Snippet: Figure 4. ULBP2 inhibits anti-tumor immunity mediated by NK cells. (A) Tumor growth in C57BL/6 mice subcutaneously transplanted with B16F10-mock cells (1 × 106). Anti-NKG2D antibody (clone HMG2D), anti-mouse CD4 antibody (clone YTS191), anti-mouse CD8α antibody (clone 2.43), or anti-mouse NK1.1 antibody (clone PK136) was administered intraperitoneally at 300 µg/mouse on day 0 post-transplantation, followed by 200 µg/mouse on days 3, 7, and 13. PBS (−) was administered as a control on the same schedule. Arrows indicate treatment days. Tumor sizes were measured three times per week using an electronic caliper (n = 5). Due to the euthanization of one mouse because of tumor ulceration, the data point for day 17 post-transplantation in the anti-NK1.1 group was unavailable. (B) Photos of tumors harvested on day 17, post-transplantation, from the experiment shown in (A). (C) Tumor weights of all tumors harvested on day 17, post-transplantation, from (A). The anti-NK1.1 group was excluded from statistical comparisons due to data loss. NA indicates exclusion from statistical comparisons. (D) Tumor growth in C57BL/6 mice subcutaneously transplanted with B16F10-ULBP2 cells (1 × 106) and treated as described in (A), except that no antibody was administered on day 13. Tumor growth was monitored as described above (n = 5). (E) Photos of tumors harvested on day 13 post-transplantation from the experiment shown in (D). (F) Tumor weights of all tumors harvested on day 13 post-transplantation from (D). (G) Schematic representation of the proposed mechanisms. A question mark and a dotted line indicate a potential mechanism suggested by our observations, but not directly demonstrated in this study. Illustration was created with BioRender.com. In (A,D), data are presented as the mean ± SEM. * p < 0.05; ** p < 0.01; ns: Not significant (Mann–Whitney U test: control vs. anti-NK1.1 group). In (C,F), individual values are shown with the mean ± SEM. * p < 0.05; ns: not significant (Mann–Whitney U test: control vs. each treatment group).

Article Snippet: NKG2D blockade, CD4+ T cell depletion, CD8+ T cell depletion, and NK cell depletion were performed by intraperitoneally administering anti-mouse NKG2D (clone HMG2D, BE0111, Bio X Cell; Lebanon, NH, USA; RRID:AB_10950118), anti-mouse CD4 (clone YTS191, BE0119, Bio X Cell; RRID:AB_10950382), anti-mouse CD8α (clone 2.43, BE0061, Bio X Cell; RRID:AB_1125541), and anti-mouse NK1.1 antibodies (clone PK136, BE0036, Bio X Cell; RRID:AB_1107737).

Techniques: Transplantation Assay, Control, MANN-WHITNEY

Journal: Phytomedicine : international journal of phytotherapy and phytopharmacology

Article Title: Compound Kushen Injection inhibits epithelial-mesenchymal transition of gastric carcinoma by regulating VCAM1 induced by the TNF signaling pathway.

doi: 10.1016/j.phymed.2023.154984

Figure Lengend Snippet: Fig. 3. CKI improves immunity in the tumor xenograft model in cooperation with DDP. (A) Mean thymus and spleen indices of different groups. (B) Representative flow cytometry images of CD3+ T cells, CD4+ T cells, CD8+ T cells in tumor tissues. (C) Representative flow cytometry images of CD3+ T cells, CD4+ T cells, CD8+ T cells in spleen tissues. (D) H & E staining of tumor sections. Data are presented as mean ± SD of 6 mice per group. *p < 0.05, **p < 0.01 vs. model group. #p < 0.05, ##p < 0.01 vs. DDP group. CKIMD, CKI middle dose; CKIHD, CKI high dose.

Article Snippet: BB515 Rat Anti-Mouse CD45 (BD, USA), APC/FireTM 750 antimouse CD3, APC anti-mouse CD4, and PE/Cyanine7 anti-mouse CD8a (BioLegend, USA) were used to label CD3+, CD4+, and CD8+ T cells, and measurement was performed by flow cytometry (Cytek, USA).

Techniques: Flow Cytometry, Staining