Journal: Signal Transduction and Targeted Therapy

Article Title: Low-dose radiotherapy synergizes with PD-1 blockade to achieve durable survival in advanced NSCLC through antitumor neutrophil programming

doi: 10.1038/s41392-026-02712-6

Figure Lengend Snippet: TRIDENT induces chemotactic and polarizing signals that recruit and program neutrophils toward an antitumor phenotype. a Schematic of the in vitro Transwell assay evaluating neutrophil migration toward tumor-conditioned medium derived from the indicated treatments. b Quantification of neutrophil migration across Transwell membranes ( n = 4 per group). c Experimental design of the in vivo neutrophil-trafficking assay in a dual-tumor model after indicated therapy. d Representative flow cytometry plots and quantification of transferred CD45.1⁺ neutrophils in tumors ( n = 7 per group). e Single-cell RNA-seq showing Cxcr2 upregulation in neutrophils from TRIDENT-treated tumors. Genes were classified as upregulated if increased in both comparisons, downregulated if decreased in both, oppositely regulated if significant in both but with opposite direction, and unchanged if non-significant in ≥1 comparison or showed minimal change. f Flow cytometric quantification of CXCR2⁺ neutrophils in second tumors in the LLC model across treatment groups ( n = 7 per group). g Heatmap comparing relative mRNA expression of Cxcl1, Cxcl2, Cxcl3 , and Cxcl5 from averaged qPCR values in tumor tissues after the indicated treatment ( n = 4 per group). Tumor growth curves ( h , i ) and survival curve ( j ) of LLC-bearing mice treated with TRIDENT alone or with CXCR2 blockade ( n = 9 per group). k, l qPCR analysis showing increased expression of Csf2 and Ifng in tumor tissues after indicated treatment ( n = 4 per group). m – p Flow cytometric analysis of antigen presentation and co-stimulatory molecules (CD14, ICAM-1, MHC-I, and CD86) on neutrophils cultured with tumor-conditioned medium derived from control, LDRT-, or HDRT-treated tumors ( n = 10 per group). Tumor growth curves ( q , r ) and survival curve ( s ) of LLC-bearing mice treated with TRIDENT alone or with GM-CSF/IFN-γ blockade ( n = 6 per group). Data are mean ± SEM. Statistical significance was assessed by one-way ANOVA ( b, f, g, k – p ), Student’s t test ( d ), two-way ANOVA ( h , i, q , r ) or log-rank test for survival ( j , s ). *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001

Article Snippet: For CXCR2 blockade, a CXCR2 antagonist (HY-101022, MedChemExpress; 2 mg/kg, i.p.) was administered every 3 days from randomization.

Techniques: In Vitro, Transwell Assay, Migration, Derivative Assay, In Vivo, Flow Cytometry, Single Cell, RNA Sequencing, Comparison, Expressing, Immunopeptidomics, Cell Culture, Control

Journal: Journal of Biomedical Science

Article Title: CXCL5 neutralization mitigates cancer cachexia by disrupting CAF-cancer cell crosstalk

doi: 10.1186/s12929-025-01192-0

Figure Lengend Snippet: A IVIS imaging of NOD-SCID mice 3 weeks post-xenograft with 1 × 10 6 human HCT 116 luc2 colon cancer cells, or 1 × 10 6 HCT 116 luc2 cancer cells plus 2 × 10 6 human colon CAF. B Mean total flux detected from the tumor at the end point (ns = not significant). C Dissected tumors and tumor mass at the 3 week endpoint. D Tumor free body weight (B.W) at the 3 week end point. E Representative images of H&E stained gastrocnemius muscle (scale bar = 50 μm). F Calculation of the myofiber cross sectional area. G qPCR analysis of CXCL1, 2, 3, 5, 6, 7, and 8 (known CXCR2 ligands) and IL-6 in the dissected tumor. H IVIS imaging of NOD-SCID mice at 3 weeks post-xenograft with human HCT 116 luc2 cancer cells plus human colon CAF, with or without CXCL5 neutralization (CXCL5 Neu Ab). I Mean total flux detected from the tumor at the 3 week end point. J Dissected tumors and tumor mass. K Tumor free body weight (B.W) at the 3 week end point. L Hanging tolerance in the treated mice. M Tibialis anterior (TA) muscle mass. N Representative H&E staining of the TA muscle (scale bar = 100 µm). O Calculation of the myofiber cross sectional area. P CXCR2 immunostaining of the TA muscle (scale bar = 100 µm). Q Proportion of CXCR2 positive myofibers. 5 mice per group were used for the experiments and the values are indicated as the mean ± SEM. For D and F * = p < 0.05 and ** = p < 0.01 indicate significantly decreased compared to PBS treated mice. For G , * = p < 0.05 indicates significantly increased compared to HCT 116 injected mice. For I – Q 5–7 mice per group were used for the experiments and the values are indicated as the mean ± SEM. * = p < 0.05 and ** = p < 0.01 indicate significantly decreased compared to vehicle alone. # = p < 0.05 and ## = p < 0.01 indicate significantly increased compared to HCT 116 plus CAF

Article Snippet: CM was treated to the differentiated myotubes for 72 h. CXCL5 neutralizing antibody MAB-254 was purchased from R&D system (MN, USA) and CXCR2 antagonist SSB225005 was obtained from MedChemExpress (NJ, USA).

Techniques: Imaging, Staining, Neutralization, Immunostaining, Injection

Journal: Journal of Biomedical Science

Article Title: CXCL5 neutralization mitigates cancer cachexia by disrupting CAF-cancer cell crosstalk

doi: 10.1186/s12929-025-01192-0

Figure Lengend Snippet: A Schematic of the protocol to investigate CXCL5 neutralization in a model of cytokine-induced skeletal muscle wasting. C57BL6/J mice were treated with 40 ng/kg CXCL5 and 80 ng/kg IL-6 for 4 weeks with or without 120 μg/kg CXCL5 neutralizing antibody. 120 μg/kg IgG1 was used as control. B Body weight at the end point of experiment. C Quadriceps muscle mass. D Gastrocnemius muscle mass. E Tibialis anterior (TA) muscle mass. F Laminin staining of the TA muscle (scale bar = 150 µm). G TA myofiber cross sectional area. H CXCR2 staining of the TA muscle (scale bar = 150 µm). I The proportion of CXCR2 positive fibers in TA muscle. J Western blot analysis of atrogin-1, MuRF-1 and CXCR2 expression in the TA muscle. K Densitometry of atrogin-1, MuRF-1 and CXCR2 expression normalized by the expression of GAPDH. For B – I, 7 mice per group were used for the experiments and for J – K, 4 mice per group were used for the experiments and the analysis was carried out two times. The values were indicated as the mean ± SEM. * = p < 0.05 and ** = p < 0.01 indicate significantly increased or decreased compared to IgG1 control. # = p < 0.05 and ## = p < 0.01 indicate significantly decreased compared to CXCL5 + IL-6 + IgG1

Article Snippet: CM was treated to the differentiated myotubes for 72 h. CXCL5 neutralizing antibody MAB-254 was purchased from R&D system (MN, USA) and CXCR2 antagonist SSB225005 was obtained from MedChemExpress (NJ, USA).

Techniques: Neutralization, Control, Staining, Western Blot, Expressing

Journal: Journal of Inflammation Research

Article Title: Mechanistic Study of CD90-Positive Synovial Fibroblasts in the Invasion and Recurrence of Pigmented Villonodular Synovitis

doi: 10.2147/JIR.S549953

Figure Lengend Snippet: Inflammatory cell infiltration is significantly higher in PVNS synovium compared to OA synovium. ( A ) Proportion of all 22 immune infiltration cells based on CIBERSORT in the dataset GSE3698 . ( B ) Boxplots visualize the differences of all 22 immune cells calculated by CIBERSORT in OA, RA and PVNS tissues in GSE3698 . ( C and D ) Immunohistochemistry image for M2 macrophages (CD206; C ) and Neutrophils (CXCR2; D ) in the synovium of the patients with OA and PVNS. Scale bar: 50µm (20X) or 20um (40X). *P < 0.05; **P < 0.01.

Article Snippet: The primary antibodies used were: mouse anti-human CD90 (1:100; Proteintech, China, 66766-1-Ig) and rabbit anti-human PDPN (1:100; Proteintech, China, 11629-1-AP) for immunofluorescence staining; mouse anti-human CD206 (1:100; Proteintech, China, 18704-1-AP) and rabbit anti-human CXCR2 (1:100; Proteintech, China, 20634-1-AP) for immunohistochemical staining.

Techniques: Immunohistochemistry