cxcl11 i tac quantikine elisa kits  (R&D Systems)

Journal: MedComm

Article Title: Inhibiting ADAR1‐Mediated Excessive Epigenetic A‐to‐I RNA Editing Improves the Immune Microenvironment and Increases Sensitivity to Immunotherapy in Lung Adenocarcinoma

doi: 10.1002/mco2.70574

Figure Lengend Snippet: Inhibition of ADAR1 enhances sensitivity to immunotherapy in the LUAD mouse model. (A) Schematic diagram of tumor construction from LLC cells, transplantation, and treatment schedule in C57BL/6J mice. (B) Images of tumors derived from sh‐LLC and control‐LLC cells treated with PD‐L1 mAb and isotype control. The groups sh‐LLC and con‐LLC refer to ADAR1‐knockdown LLC cells prepared using shRNA and control LLC cells, respectively. n = 5 mice per group. (C) Tumor growth curves for the four groups. n = 5 mice per group. (D) IHC images of CD8 and PD‐L1 expression in the corresponding groups. (E, F) IHC analysis of CD8 + T‐cell infiltration in the corresponding groups. (G–K) ELISA analysis of IFN‐β, IFN‐γ, CXCL9, CXCL10, and CXCL11 concentrations in the corresponding groups. (L–O) IHC analysis of IFN‐β, CXCL9, CXCL10, and CXCL11 expression in the corresponding groups (* p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001; t ‐test; error bars represent standard deviation).

Article Snippet: Primary antibodies for IHC staining included ADAR1 (Abcam, #88574), ADAR2 (Santa Cruz, #sc‐73409), CD8 (Zsbio Tech, #ZA‐0508), PD‐L1 (Ventana, #740‐4907), IFN‐β (Abcam, #140211), CXCL9 (Proteintech, #22355‐1‐AP), CXCL10 (R&D, #MAB2662), and CXCL11 (Proteintech, #10707‐1‐AP).

Techniques: Inhibition, Transplantation Assay, Derivative Assay, Control, Knockdown, shRNA, Expressing, Enzyme-linked Immunosorbent Assay, Standard Deviation

Journal: MedComm

Article Title: Inhibiting ADAR1‐Mediated Excessive Epigenetic A‐to‐I RNA Editing Improves the Immune Microenvironment and Increases Sensitivity to Immunotherapy in Lung Adenocarcinoma

doi: 10.1002/mco2.70574

Figure Lengend Snippet: ADAR1 suppressed the activation of TME and led to poor prognosis in LUAD. (A) IHC analysis of CD8 + TILs in tissue samples from 227 LUAD patients. ADAR1‐low and ADAR1‐high refer to the low‐ADAR1‐expression and high‐expression groups, respectively, based on the median IHC score. (B) IHC analysis of PD‐L1 in tissue samples from 227 LUAD patients. (C) Percentage of TME types in 227 LUAD patients. (D) IHC analysis of IFN‐β in tissue samples from 227 LUAD patients. (E) IHC analysis of CXCL9 in tissue samples from 227 LUAD patients. (F) IHC analysis of CXCL10 in tissue samples from 227 LUAD patients. (G) IHC analysis of CXCL11 in tissue samples from 227 LUAD patients. (H) CD8 + TILs in the low‐ and high‐editing‐level groups of 32 frozen surgical specimens. (I) PD‐L1 expression in the low‐ and high‐editing‐level groups of 32 frozen surgical specimens. (J) Correlation between ADAR1 expression and A‐to‐I editing level in 32 LUAD patients. (K) Survival analysis of 227 LUAD patients in low‐ and high‐ADAR1‐expression groups (*** p < 0.001; **** p < 0.0001; chi‐square test; t ‐test; error bars represent standard deviation).

Article Snippet: Primary antibodies for IHC staining included ADAR1 (Abcam, #88574), ADAR2 (Santa Cruz, #sc‐73409), CD8 (Zsbio Tech, #ZA‐0508), PD‐L1 (Ventana, #740‐4907), IFN‐β (Abcam, #140211), CXCL9 (Proteintech, #22355‐1‐AP), CXCL10 (R&D, #MAB2662), and CXCL11 (Proteintech, #10707‐1‐AP).

Techniques: Activation Assay, Expressing, Standard Deviation