Fig 1: Protein expression of NKG2D in the parietal cortex and spleen from patients with major psychiatric disorders. a Parietal cortex: There were no changes (one-way ANOVA, F3,53 = 3.004, P = 0.051) among the four groups. The bands of representative bands of Western blot analysis were shown. Data are shown as mean ± SEM. (n = 15). b Spleen: There were significant changes (one-way ANOVA, F3,52 = 2.673, P = 0.048) among the four groups. Expression of NKG2D in the spleen of MDD patients was significantly (P = 0.012) higher than controls. *P < 0.05. Data are shown as mean ± SEM. (n = 12–15). The bands of representative bands of Western blot analysis were shown. CON control, MDD major depressive disorder, SZ schizophrenia, BD bipolar disorder, N.S. not significant
Fig 2: CDX2/CXCL14 inhibits the growth of head and neck squamous cell carcinoma (HNSCC) in vivo. (A) RT-qPCR to detect the expression of CDX2 and CXCL14 in tumours. (B) The measurement of tumour volume. (C) The measurement of tumour weight. (D) IF to detect the NK cell infiltration in tumours. (E) Western blot assay to analyse the expression of NKG2D in mouse tumours. *P < .05 compared with sh-NC group, and # P < .05 compared with sh-mCDX2 + oe-NC group. Tumours were excised 3 wks after lentivirus injection, and RT-qPCR, IF and Western blot assay were performed. Measurement data were presented as mean ± standard deviation. Data among multiple groups were processed via one-way ANOVA and Tukey's post hoc test, and tumour volume data from different time-points were analysed by repeated measures ANOVA. Experiments were repeated 3 times
Fig 3: Immunohistochemical staining of NKG2D, CD56, and MICA/B in ovarian serous carcinoma. (A and B) A representative image of ovarian serous carcinoma showing NKG2D- (A) and CD56 (B)-positive cells (×200). NKG2D- and CD56-positive cells at high magnification (small boxes). These cells were present mainly in the intratumoral area. (C-F) MICA/B staining of ovarian serous carcinoma. Intensity score: 0 (C), 1+ (D), 2+ (E), and 3+ (F) (×100). MICA/B is expressed mainly on the membrane of tumor cells. When 50% or more tumor cells were positively stained and the intensity was 1+ or more, it was considered as high expression.
Fig 4: CXCL14 inhibits the growth of head and neck squamous cell carcinoma (HNSCC) in vivo. (A) RT-qPCR to detect CXCL14 expression in mouse tumours. (B) Measurement of tumour volume. (C) Measurement of tumour weight. (D) IF to detect the NK cell infiltration in mouse tumours. (E) Western blot assay to analyse the expression of NKG2D in mouse tumours. ^P < .05 compared with blank group, *P < .05 compared with oe-NC group, # P < .05 compared with oe-mCXCL14 group, and & P < .05 compared with sh-NC group. Tumours were excised 3 wks after lentivirus injection, and RT-qPCR, IF and Western blot assay were performed. Measurement data were presented as mean ± standard deviation. Data among multiple groups were compared via one-way ANOVA and Tukey's post hoc test, and tumour volume data from different time-points were analysed by repeated measures ANOVA. Experiments were repeated 3 times
Fig 5: CDX2 enhances NK cell migration and cytolytic activity via up-regulating CXCL14 expression. (A) Transwell assay to detect the effect of CXCL14 on the migration of NK cells. (B) ELISA to measure the levels of IFN-? and TNF-a in the medium of NK cells. (C) Western blot assay to analyse the expression of NKG2D and PD-1 in NK cells. (D) The cytotoxicity of NK cells to head and neck squamous cell carcinoma (HNSCC) cell line CAL27. (E) The cytotoxicity of NK cells to HNSCC cell line SCC-25. (F) Immunohistochemistry to detect the expression of CD45 in SCC-25 tumour spheroid. *P < .05 compared with oe-NC, # P < .05 compared with sh-NC group, and & P < .05 compared with sh-CDX2 + oe-NC group. Measurement data were presented as mean ± standard deviation. Data of two groups were compared using unpaired t test. Experiments were repeated 3 times
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