Journal: PLOS One

Article Title: Bulk and single-cell RNA-sequencing analyses revealed potential key genes and the role of CCL19/CCL21-CCR7 axis in hidradenitis suppurativa

doi: 10.1371/journal.pone.0322565

Figure Lengend Snippet: A. CCR7 gene expression in HS lesion. B. Serum levels of CCL19 and CCL21 (n = 8). C. Correlation analysis between CCL19 and CCL21 in the skin and Treg cells in the blood. D. HS and healthy control average gene expression of Treg cluster. E. Flow cytometric analysis of CCR7 + lymphocytes percentages within lymphocytes compartment and Treg percentages within the CD4 + T cell compartment (n = 3). F. The CLL19 and CLL21 genes expression analysis in the HS cell subset clusters. (*P < 0.05, **P < 0.01, ***P < 0.005, ****P < 0.001).

Article Snippet: Plasma levels of CCL19 (BOSTER, EK0456) and CCL21 (BOSTER, EK0555) were quantified using a commercially available ELISA kits according to the manufacturer’s protocol.

Techniques: Gene Expression, Control, Expressing

Journal: The Journal of Pathology

Article Title: Loss of RUNX3 expression promotes cancer‐associated bone destruction by regulating CCL5 , CCL19 and CXCL11 in non‐small cell lung cancer

doi: 10.1002/path.4597

Figure Lengend Snippet: RUNX3 knockdown in NSCLC cells substantially increased the osteoblastic RANKL/OPG ratio by modulating NSCLC‐derived chemokines. (A, B) The mRNA levels of RANKL and OPG were determined via qRT‐PCR in hFOB1.19 cells treated with 50% and 75% CM from shNC or shRUNX3 A549 (A) and H838 cells (B) for 6 h. Mean ± SE; # p < 0.05, ## p < 0.01 versus osteoblastic cells without CM; * p < 0.05 versus osteoblastic cells treated with shNC cell‐derived CM. (C) CCL5, CCL19, and CXCL11 in culture media of shNC or shRUNX3 A549 and H838 cells. Mean ± SE; * p < 0.05 versus shNC cells. (D, E) hFOB1.19 osteoblastic cells were treated with 75% CM of A549 cells (D) or H838 cells (E) and the indicated concentrations of neutralizing antibodies against CCL5, CCL19 or CXCL11 for 6 h. RANKL and OPG protein were investigated via western blot analysis. The images are representative of three independent experiments. The graphs illustrate the ratio of the densitometric intensity of RANKL to that of OPG after normalization to β‐actin. Mean ± SE; # p < 0.01 versus osteoblastic cells without CM and specific antibodies against chemokines; * p < 0.05 versus CM‐treated osteoblastic cells.

Article Snippet: CCL5, CCL19, and CXCL11 levels in CM were measured with Quantikine human CCL5/RANTES and CXCL11/I‐TAC immunoassay kits (R&D Systems, Minneapolis, MN, USA) and the CCL19 ELISA kit (Abnova, Taipei City, Taiwan) following the manufacturers' protocols.

Techniques: Knockdown, Derivative Assay, Quantitative RT-PCR, Western Blot

Journal: The Journal of Pathology

Article Title: Loss of RUNX3 expression promotes cancer‐associated bone destruction by regulating CCL5 , CCL19 and CXCL11 in non‐small cell lung cancer

doi: 10.1002/path.4597

Figure Lengend Snippet: RUNX3 knockdown promoted tumour growth and caused bone destruction in mouse calvaria inoculated with NSCLC cells. shNC or shRUNX3 A549 cells (1 × 10 7 per 100 µl of PBS) were injected subcutaneously over the calvaria. Control mice were injected with PBS alone. On day 46, blood was collected and the mice were euthanized. (A) Tumour volumes and photos of tumour‐bearing mouse heads. (B) H&E and TRAP staining of calvarial tissues. T = tumour; B = bone; Br = brain. Arrowheads denote osteoclasts (original magnification × 100). (C) 3D images were reconstructed from the 2D images of μCT using the software supplied with the instrument. (D) Bone morphometric parameters BV/TV (%) and BS/TV (1/mm) in mouse calvaria using μCT. (E) Serum levels of bone turnover markers Ca 2+ , ALP, and TRAP5b, and (F) RUNX3‐regulated chemokines. (G) Immunohistochemical analyses of RUNX3, CCL5, CCL19, and CXCL11 in the tumour tissues of mouse calvaria (original magnification × 200). Means ± SE. * p < 0.05, ** p < 0.005 versus shNC A549 cell‐inoculated mice.

Article Snippet: CCL5, CCL19, and CXCL11 levels in CM were measured with Quantikine human CCL5/RANTES and CXCL11/I‐TAC immunoassay kits (R&D Systems, Minneapolis, MN, USA) and the CCL19 ELISA kit (Abnova, Taipei City, Taiwan) following the manufacturers' protocols.

Techniques: Knockdown, Injection, Control, Staining, Software, Immunohistochemical staining

Journal: The Journal of Pathology

Article Title: Loss of RUNX3 expression promotes cancer‐associated bone destruction by regulating CCL5 , CCL19 and CXCL11 in non‐small cell lung cancer

doi: 10.1002/path.4597

Figure Lengend Snippet: RUNX3 knockdown aggravated bone destruction in mouse tibiae inoculated with NSCLC cells. A549 cells (1 × 10 6 cells per 50 µl of HBSS) were injected into the bone marrow of the tibiae through the femorotibial cartilage. Control mice were injected with HBSS alone. On day 49, the mouse tibiae were analysed using μCT and blood and tibiae were collected. (A) Radiophotographs and 3D images of μCT data from the tibiae. Arrowheads indicate osteolytic foci. (B) The bone morphometric parameters of mouse tibia were determined using μCT. (C) H&E (original magnification × 50) and TRAP staining (original magnification × 100). Tumour area was measured in H&E‐stained tissues. T = tumour; B = bone. Arrowheads denote osteoclasts (D, E) Serum levels of bone turnover markers Ca 2+ , ALP, and TRAP5b, and RUNX3‐regulated chemokines. (F) RUNX3, CCL5, CCL19, and CXCL11 in tumour tissues of mouse tibiae were detected via immunohistochemical analysis (original magnification × 200). Means ± SE. # p < 0.05, ## p < 0.005 versus control mice; * p < 0.05 versus shNC A549 cell‐inoculated mice.

Article Snippet: CCL5, CCL19, and CXCL11 levels in CM were measured with Quantikine human CCL5/RANTES and CXCL11/I‐TAC immunoassay kits (R&D Systems, Minneapolis, MN, USA) and the CCL19 ELISA kit (Abnova, Taipei City, Taiwan) following the manufacturers' protocols.

Techniques: Knockdown, Injection, Control, Staining, Immunohistochemical staining

Journal: The Journal of Pathology

Article Title: Loss of RUNX3 expression promotes cancer‐associated bone destruction by regulating CCL5 , CCL19 and CXCL11 in non‐small cell lung cancer

doi: 10.1002/path.4597

Figure Lengend Snippet: CCL5 enhanced the proliferation, migration, and invasion of NSCLC cells. (A) Trypan blue exclusion of A549 (1 × 10 5 cells per ml) treated with the indicated concentrations of human CCL5, CCL19, or CXCL11 for 48 h. (B) BrdU incorporation of cells (1 × 10 4 cells per well) exposed to the indicated concentrations of chemokines for 24 h. (C) Cell migration in RPMI1640 medium containing 2% FBS, 10 µg/ml mitomycin C, and the indicated concentrations of chemokines for 24 h. (D) A549 (1 × 10 5 cells per 0.1 ml) invasion through Matrigel‐coated filter. Cells were suspended in serum‐free medium containing 0.01% BSA. The lower chamber was filled with 600 µl of medium containing 10% FBS and/or human chemokines at the indicated concentrations. Invaded cells were counted after 48 h. Means ± SE. # p < 0.05, ## p < 0.005 versus cells without chemokines; * p < 0.05, ** p < 0.005 versus shNC cells.

Article Snippet: CCL5, CCL19, and CXCL11 levels in CM were measured with Quantikine human CCL5/RANTES and CXCL11/I‐TAC immunoassay kits (R&D Systems, Minneapolis, MN, USA) and the CCL19 ELISA kit (Abnova, Taipei City, Taiwan) following the manufacturers' protocols.

Techniques: Migration, BrdU Incorporation Assay

Journal: The Journal of Pathology

Article Title: Loss of RUNX3 expression promotes cancer‐associated bone destruction by regulating CCL5 , CCL19 and CXCL11 in non‐small cell lung cancer

doi: 10.1002/path.4597

Figure Lengend Snippet: CCL5, CCL19, and CXCL11 altered RANKL and OPG expression in osteoblastic cells and RANKL‐induced osteoclast differentiation in BMMs. Human osteoblastic hFOB1.19 cells were treated with the indicated concentrations of human CCL5, CCL19, or CXCL11 for 6 h. (A) RANKL and OPG mRNA analysed via qRT‐PCR. GAPDH was used as an endogenous control. (B) Western blots of total cell lysates (representative of three independent experiments). β‐actin served as a loading control. Graphs show densitometric intensity ratios of RANKL/OPG after normalization. Means ± SE; * p < 0.01 versus osteoblastic cells without chemokines. (C) Mouse BMMs (5 × 10 4 cells per well) cultured for 5 days in α‐MEM containing 10% FBS and 30 ng/ml M‐CSF, in the absence or presence of CCL5, CCL19, or CXCL11 at the indicated concentrations and in the absence (control) or presence of 100 ng/ml RANKL. TRAP staining was performed to detect osteoclasts (original magnification × 100). TRAP‐positive multinucleated cells (≥3 nuclei) were counted as osteoclasts. Means ± SE; * p < 0.05, ** p < 0.005 versus RANKL‐treated BMMs.

Article Snippet: CCL5, CCL19, and CXCL11 levels in CM were measured with Quantikine human CCL5/RANTES and CXCL11/I‐TAC immunoassay kits (R&D Systems, Minneapolis, MN, USA) and the CCL19 ELISA kit (Abnova, Taipei City, Taiwan) following the manufacturers' protocols.

Techniques: Expressing, Quantitative RT-PCR, Control, Western Blot, Cell Culture, Staining

Journal: Journal of immunology (Baltimore, Md. : 1950)

Article Title: Immunization with HSV-2 gB-CCL19 Fusion Constructs Protects Mice against Lethal Vaginal Challenge.

doi: 10.4049/jimmunol.1500198

Figure Lengend Snippet: FIGURE 1. Design and expression of HSV-2 gB-CCL19 fusion constructs and immunization schedule. (A) Schematic representation of the pgBIZCCL19 and pCCL19IZgB constructs. The fusion linker contains an IZ and two (G4S)2 motifs for trimerization and stabilization. (B) Expression analysis of gB. Supernatants from 293T cells transfected with the indicated constructs were collected and resolved by denatured SDS-PAGE and native PAGE, followed by Western blotting. (C) Expression analysis of CCL19. Supernatants from 293T cells transfected with the indicated constructs were collected and analyzed by ELISA. Culture supernatants from pcDNA3.1 transfected cells were used as negative controls. Data are mean 6 SEM of at least three independent experiments, performed in triplicate for each condition. (D) Intramuscular immunization and i.vag. challenge schedule. Mice were immunized twice with pcDNA3.1, pgB, pgB plus pCCL19, or gB-CCL19 fusion constructs in saline solution at days 0 and 14. Fourteen days postboost, all mice were sampled. Forty-nine days postboost, some mice were sacrificed for tissue collection, whereas the rest were used for the challenge experiments. Postchallenge, the weight and clinical symptoms of all mice were monitored every day for 15 d. Sera, vaginal fluids, and sacral ganglia were collected for subsequent tests.

Article Snippet: Forty-eight hours posttransfection, the protein-containing supernatants were harvested for gB and CCL19 quantification. gB was detected by Western blotting, whereas CCL19 concentration was measured by ELISA using commercial mouse CCL19 DuoSet ELISA kits (R&D Systems), according to the manufacturer’s instructions.

Techniques: Expressing, Construct, Transfection, SDS Page, Clear Native PAGE, Western Blot, Enzyme-linked Immunosorbent Assay, Saline

Journal: Journal of immunology (Baltimore, Md. : 1950)

Article Title: Immunization with HSV-2 gB-CCL19 Fusion Constructs Protects Mice against Lethal Vaginal Challenge.

doi: 10.4049/jimmunol.1500198

Figure Lengend Snippet: FIGURE 6. The chemotactic activity of CCL19. (A and B) IgA+ cell number at the colorectal mucosal sites of immunized mice. Mouse colorectal samples were collected at day 14 postboost, and IgA+ cells were detected by immunohistochemistry. The colorimetric reaction was developed with the addition of diaminobenzidine and counterstained with H&E. (A) Representative results (original magnification 3200). (B) Quantification of IgA+ cells by counting five high-power fields for each mouse. Data are mean 6 SEM. (C) Migration of splenocytes and MLNLs from immunized mice in response to murine CCL19. Single cells were prepared and counted to assess chemotactic response to CCL19 using a Transwell system. The migrated cells in lower chamber were counted after a 2-h incubation. Fold change was calculated compared with the cell number in the lower chamber without CCL19. Data in (B) and (C) are mean 6 SEM for each group (n = 5 mice/group). **p , 0.01, ***p , 0.001.

Article Snippet: Forty-eight hours posttransfection, the protein-containing supernatants were harvested for gB and CCL19 quantification. gB was detected by Western blotting, whereas CCL19 concentration was measured by ELISA using commercial mouse CCL19 DuoSet ELISA kits (R&D Systems), according to the manufacturer’s instructions.

Techniques: Activity Assay, Immunohistochemistry, Migration, Incubation

Journal: BMC Veterinary Research

Article Title: MIP-3β/CCL19 is associated with the intrathecal invasion of mononuclear cells in neuroinflammatory and non-neuroinflammatory CNS diseases in dogs

doi: 10.1186/1746-6148-10-157

Figure Lengend Snippet: CSF and serum characteristics in patients with IE, neuroinflammatory disease, IVDD and clinically healthy patients

Article Snippet: An ELISA Kit specific for canine CCL19 (E90096Ca 96 Tests) was used according to manufacturer’s instructions (Uscn Life Science Inc., Wuhan, P.R.

Techniques: Control

Journal: BMC Veterinary Research

Article Title: MIP-3β/CCL19 is associated with the intrathecal invasion of mononuclear cells in neuroinflammatory and non-neuroinflammatory CNS diseases in dogs

doi: 10.1186/1746-6148-10-157

Figure Lengend Snippet: CCL19 CSF concentrations of patients with SRMA compared to the control group. y- axis: logarithm to base 10 of CCL19 (pg/ml); x- axis: groups. Boxes contain values from the 1st to the 3rd quartile, lines inside boxes indicate median values, endpoints of vertical lines display minimum and maximum values, o represents the outliers. Asterisks indicate statistically significant differences (* P < 0.05; ** P < 0.01; *** P < 0.005). SRMA = steroid-responsive meningitis-arteritis; CSF = cerebrospinal fluid; IE = idiopathic epilepsy.

Article Snippet: An ELISA Kit specific for canine CCL19 (E90096Ca 96 Tests) was used according to manufacturer’s instructions (Uscn Life Science Inc., Wuhan, P.R.

Techniques: Control

Journal: BMC Veterinary Research

Article Title: MIP-3β/CCL19 is associated with the intrathecal invasion of mononuclear cells in neuroinflammatory and non-neuroinflammatory CNS diseases in dogs

doi: 10.1186/1746-6148-10-157

Figure Lengend Snippet: CCL19 CSF concentrations of patients with MUO compared to the control group. y- axis: logarithm to base 10 of CCL19 (pg/ml); x- axis: groups. Boxes contain values from the 1st to the 3rd quartile, lines inside boxes indicate median values, endpoints of vertical lines display minimum and maximum values, o represents the outliers. Asterisks indicate statistically significant differences (* P < 0.05; ** P < 0.01; *** P < 0.005). MUO = meningoencephalomyelitis of unknown origin; CSF = cerebrospinal fluid; IE = idiopathic epilepsy.

Article Snippet: An ELISA Kit specific for canine CCL19 (E90096Ca 96 Tests) was used according to manufacturer’s instructions (Uscn Life Science Inc., Wuhan, P.R.

Techniques: Control

Journal: BMC Veterinary Research

Article Title: MIP-3β/CCL19 is associated with the intrathecal invasion of mononuclear cells in neuroinflammatory and non-neuroinflammatory CNS diseases in dogs

doi: 10.1186/1746-6148-10-157

Figure Lengend Snippet: CCL19 CSF concentrations of patients with IVDD compared to the control group. Boxes contain values from the 1st to the 3rd quartile, lines inside boxes indicate median values, endpoints of vertical lines display minimum and maximum values, o represents the outliers. Asterisks indicate statistically significant differences (* P < 0.05; ** P < 0.01; *** P < 0.005). IVDD = intervertebral disc disease; CSF = cerebrospinal fluid; IE = idiopathic epilepsy.

Article Snippet: An ELISA Kit specific for canine CCL19 (E90096Ca 96 Tests) was used according to manufacturer’s instructions (Uscn Life Science Inc., Wuhan, P.R.

Techniques: Control

Journal: iScience

Article Title: CCL19-armed recombinant influenza virus inhibited colorectal cancer growth by remodeling tumor microenvironment

doi: 10.1016/j.isci.2025.114127

Figure Lengend Snippet: Generation and characterization of recombinant PR8-CCL19 ( r PR8-CCL19) (A) Schematic design of r PR8-CCL19 via insertion of the CCL19 gene into the 3′ terminal region of the PB1 gene of the PR8 influenza virus strain. (B) The H&A titer of P1 r PR8-CCL19 (1:128) detected by hemagglutination assay. P1, passage 1 of r PR8-CCL19; wt PR8, wild-type PR8. (C) Real-time PCR amplification of CCL19 gene (target fragment size:∼700 and ∼300 bp) was to identify genetic stability of r PR8-CCL19. M, 1,000 bp DNA marker; P1–P5, passage 1–5 of r PR8-CCL19; wt PR8, wild-type PR8. (D) Quantification of HA titers of P1–P5 r PR8-CCL19. Data were analyzed with descriptive statistical method and represented as mean ± SEM. n represents technical replicates, n = 3. (E) The CCL19 expression and secretion in chicken embryos infected with P1–P5 r PR8-CCL19 detected through ELISA. Data were analyzed with descriptive statistical method and represented as mean ± SEM. n represents technical replicates, n = 3. (F) Transmission electron microscopy image showed the morphology of r PR8-CCL19. Scale bars, 200 nm. (G) Transmission electron microscopy image showed the morphology of wt PR8. Scale bars, 200 nm.

Article Snippet: Human CCL19 ELISA Kit , Beijing 4A Biotech , HUEB0059.

Techniques: Recombinant, Virus, Hemagglutination Assay, Real-time Polymerase Chain Reaction, Amplification, Marker, Expressing, Infection, Enzyme-linked Immunosorbent Assay, Transmission Assay, Electron Microscopy

Journal: iScience

Article Title: CCL19-armed recombinant influenza virus inhibited colorectal cancer growth by remodeling tumor microenvironment

doi: 10.1016/j.isci.2025.114127

Figure Lengend Snippet: The replication and tumor cell-killing activity of r PR8-CCL19 in vitro (A) The proliferation dynamics of r PR8-CCL19 in various CRC cell lines (CT26, HT29, HCT116, SW620, and Lovo) and the normal colonic mucosal epithelial cell line CCD841, as determined by the HA titter measurement. Data were analyzed with descriptive statistical method and represented as mean ± SEM. n represents technical replicates, n = 3. (B) Cell killing study performed through xCELLigence RTCA representing individual cell impedance measurements of cells in real time in response to the treatment with r PR8-CCL19, wt PR8, and r CCL19, respectively. The control group (CON) with non-treatment was also applied. (C) The flow cytometric analysis of apoptosis in HT29 cells infected with r PR8-CCL19 and wt PR8 at 24, 48, and 72 h post-infection, respectively. The CON with non-treatment was also applied. (D) Quantification of HT29 cells apoptotic ratio. r PR8-CCL19 induced more than 78% cell apoptosis at 24 h post-infection. Data were analyzed with unpaired two-sided Student’s t test and represented as mean ± SEM. n represents technical replicates, n = 3. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. (E) Detection of changes in mitochondrial membrane potential (MMP) in HT29 cells at 24 h post-infection with r PR8-CCL19 by flow cytometry, compared with wt PR8 and CON. (F) Quantification of MMP in HT29 cell. MMP decreased significantly after r PR8-CCL19 treatment. Data were analyzed with unpaired two-sided Student’s t test and represented as mean ± SEM. n represents technical replicates, n = 3. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. (G) The expressions of PARP, caspase-3, caspase-9, caspase-8, and their corresponding cleavers in HT29 cells infected with r PR8-CCL19 or wt PR8 were detected by western blotting, respectively. (H) The expressions of BAX, Bcl-2, cyto-cyc (cytochrome in cytoplasm), and mito-cyc (cytochrome in mitochondria) in HT29 cells infected with r PR8-CCL19 or wt PR8 were detected by western blotting, respectively.

Article Snippet: Human CCL19 ELISA Kit , Beijing 4A Biotech , HUEB0059.

Techniques: Activity Assay, In Vitro, Control, Infection, Membrane, Flow Cytometry, Western Blot

Journal: iScience

Article Title: CCL19-armed recombinant influenza virus inhibited colorectal cancer growth by remodeling tumor microenvironment

doi: 10.1016/j.isci.2025.114127

Figure Lengend Snippet: The abilities of r PR8-CCL19 expressing CCL19, chemotacticing immune cells, and activating them in vitro (A) The expression and secretion of CCL19 were detected by ELISA in various colorectal cancer cells infected with r PR8-CCL19 at 72 h post-infection. Data were analyzed with unpaired two-sided Student’s t test and represented as mean ± SEM. n represents technical replicates, n = 3. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. (B) Chemotactic effect of CCL19 secreted by rPR8-CCL19-infected colorectal cancer cells on immature dendtric cells ( i DCs) was detected by transwell assay. (C) Quantification of the number of i DCs migrating to the lower chamber in the transwell assay. Data were analyzed with one-way ANOVA and represented as mean ± SEM. n represents technical replicates, n = 3. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. (D) The CD11c + MHC-II + DCs were analyzed using flow cytometry. (E) The CD11c + CD86 + DCs were analyzed using flow cytometry. (F) The CD11c + CD80 + DCs were analyzed using flow cytometry. (G) Quantitative analysis of CD11c + MHC + II DCs, CD11c + CD86 + DCs, and CD11c + CD80 + DCs, respectively. Data were analyzed with one-way ANOVA and represented as mean ± SEM. n represents technical replicates, n = 3. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

Article Snippet: Human CCL19 ELISA Kit , Beijing 4A Biotech , HUEB0059.

Techniques: Expressing, In Vitro, Enzyme-linked Immunosorbent Assay, Infection, Transwell Assay, Flow Cytometry

Journal: iScience

Article Title: CCL19-armed recombinant influenza virus inhibited colorectal cancer growth by remodeling tumor microenvironment

doi: 10.1016/j.isci.2025.114127

Figure Lengend Snippet: Evaluation of r PR8-CCL19 anti-tumor activity and safety in unilateral CT26-bearing mouse model (A) Schedule of the animal experiment using the CT26 tumor model. (B) Tumor volume growth curves of subcutaneous transplanted tumors of CT26 in BABL/C mice treated with PBS (10 μL/mouse), wt PR8 (10 μL 1 × 10 5 PFU/mouse), r PR8-CCL19(10 μL 1 × 10 5 PFU/mouse) and r CCL19(0.2μg/mouse), respectively, after 11 and 21 days post-treatment. Data were analyzed with two-way ANOVA and represented as mean ± SEM. n represents the number of animals, n = 6. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. (C) The macroscopic images of the subcutaneous transplanted tumors and corresponding tumor weights. Data were analyzed with one-way ANOVA and represented as mean ± SEM. n represents the number of animals, n = 6. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. (D) The body weight changes curves of tumor-bearing BABL/C mice after 11 and 21 days post-treatment. Data were analyzed with two-way ANOVA and represented as mean ± SEM. n represents the number of animals, n = 6. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. (E) The Kaplan-Meier survival curves of tumor-bearing mice in four experiment groups over an 80-day observation. Data were analyzed with the Kaplan-Meier method. n represents the number of animals, n = 6. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. (F) The macroscopic images of lungs from tumor-bearing mice and corresponding lung wet weight. Data were analyzed with one-way ANOVA and represented as mean ± SEM. n represents the number of animals, n = 6. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. (G) The histological sections of mouse lung tissues at 11th and 21st day post-treatment were stained by H&E. r PR8-CCL19 could not cause pathological injury. Scale bars, 100 μm. (H) The viral bio-distribution at 11th and 21st day post-treatment in tumor-bearing mice by real-time PCR for detection of influenza virus M gene expression in vivo . Data were analyzed with unpaired two-sided Student’s t test and represented as mean ± SEM. n represents the number of animals, n = 6. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. (I) The inhibitory effect of r PR8-CCL19 on lung metastatic CT26 tumors and quantification of the number of tumor foci per mouse. Data were analyzed with one-way ANOVA and represented as mean ± SEM. n represents the number of animals, n = 4. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001).

Article Snippet: Human CCL19 ELISA Kit , Beijing 4A Biotech , HUEB0059.

Techniques: Activity Assay, Staining, Real-time Polymerase Chain Reaction, Virus, Gene Expression, In Vivo

Journal: iScience

Article Title: CCL19-armed recombinant influenza virus inhibited colorectal cancer growth by remodeling tumor microenvironment

doi: 10.1016/j.isci.2025.114127

Figure Lengend Snippet: The TME was remodeled by r PR8-CCL19 virus after oncolytic treatment in vivo (A) Histological sections of tumor tissues were stained by H&E. Scale bars, 100 μm. (B) Histological sections of tumor tissues were stained with anti-CD8 (pink), anti-CD4 (red), and anti-CD3 (green) antibodies for the fluorescence microscopy (scale bars, 1000 μm/50 μm), along with the corresponding quantification of the ratio of total T cells, CD4 + T cells, CD8 + T cells infiltrating in the TME at the 11th day post-treatment. Data were analyzed with one-way ANOVA and represented as mean ± SEM. n represents the number of animals, n = 6. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. (C) Histological sections of tumor tissues were stained with anti-CD8 (pink), anti-CD4 (red), and anti-CD3 (green) antibodies for the fluorescence microscopy (scale bars, 1000 μm/50 μm), along with corresponding quantification of the ratio of total T cells, CD4 + T cells, CD8 + T cells infiltrating in TME at the 21st day post-treatment. Data were analyzed with one-way ANOVA and represented as mean ± SEM. n represents the number of animals, n = 6. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. (D) The mRNA expression of Granzyme B, perforin, IL-2, IFN-γ, and CCL19 in TME was detected by real-time PCR at the 11th day post-treatment. Data were analyzed with one-way ANOVA and represented as mean ± SEM. n represents the number of animals, n = 6. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. (E) The mRNA expression of Granzyme B, perforin, IL-2, IFN-γ, and CCL19 in TME was detected by real-time PCR at the 21st day post-treatment. Data were analyzed with one-way ANOVA and represented as mean ± SEM. n represents the number of animals, n = 6. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

Article Snippet: Human CCL19 ELISA Kit , Beijing 4A Biotech , HUEB0059.

Techniques: Virus, In Vivo, Staining, Fluorescence, Microscopy, Expressing, Real-time Polymerase Chain Reaction

Journal: iScience

Article Title: CCL19-armed recombinant influenza virus inhibited colorectal cancer growth by remodeling tumor microenvironment

doi: 10.1016/j.isci.2025.114127

Figure Lengend Snippet: Evaluation of activation of systemic anti-tumor immunity and immune memory in vivo (A) The flow cytometry was employed to evaluate the differentiation and development of immune cells in unilateral CT26-bearing mouse models at the 11th day post-oncolytic treatment. Data were analyzed with one-way ANOVA and represented as mean ± SEM. n represents the number of animals, n = 6. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. (B) The flow cytometry was employed to evaluate the differentiation and development of immune cells in unilateral CT26-bearing mouse models at the 21st day post-oncolytic treatment. Data were analyzed with one-way ANOVA and represented as mean ± SEM. n represents the number of animals, n = 6. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. (C) The growth curves of the injected and non-injected tumors (distant tumors). The injected tumors were treated with PBS (10 μL/mouse), wt PR8 (10 μL 1 × 10 5 PFU/mouse), r PR8-CCL19(10 μL 1 × 10 5 PFU/mouse), and r CCL19(0.2μg/mouse). The distant tumors were untreated. Data were analyzed with two-way ANOVA and represented as mean ± SEM. n represents the number of animals, n = 6. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. (D) The Kaplan-Meier survival curves of bilateral tumor-bearing mice models in each experimental group. Data were analyzed with the Kaplan-Meier method. n represents the number of animals, n = 6. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. (E) Tumors growth curves in tumor rechallenge models. The mice treated with r PR8-CCL19 prevented tumor growth upon re-tumorigenesis due to the induction of robust immune memory. Data were analyzed with descriptive statistical method. n represents the number of animals, n = 3. (F) The Kaplan-Meier survival curves of tumor re-challenge mice models in the r PR8-CCL19 treatment group and CON group. Data were analyzed with the Kaplan-Meier method. n represents the number of animals, n = 3. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. (G) The serum hemagglutination inhibition (HI) titers in each group. r PR8-CCL19 and wt PR8 groups induced anti-influenza virus immunity at 11th and 21st days after oncolytic therapy in unilateral tumor-bearing mouse models. Data were analyzed with one-way ANOVA and represented as mean ± SEM. n represents thne number of animals, n = 6. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

Article Snippet: Human CCL19 ELISA Kit , Beijing 4A Biotech , HUEB0059.

Techniques: Activation Assay, In Vivo, Flow Cytometry, Injection, HI Assay, Virus

Journal: Journal of Ginseng Research

Article Title: Reciprocal regulation of SIRT1 and AMPK by Ginsenoside compound K impedes the conversion from plasma cells to mitigate for podocyte injury in MRL/ lpr mice in a B cell-specific manner

doi: 10.1016/j.jgr.2023.11.006

Figure Lengend Snippet: CK alleviated lupus manifestations. (A) Chemical structure of CK. (B) Experimental scheme. (C) Overall survival curve. (D) Representative spleens and spleen indexes. (E) The levels of anti-dsDNA antibody. (F) The levels of TNF-α, IL-6, and IL-10. (G) The levels of CXCL12, CXCL13, and CCL19 in serum.

Article Snippet: Concentrations of TNF-α, IL-6, IL-10, CXCL12, CXCL13, CCL19, and anti-dsDNA were assessed using corresponding ELISA kits (Cusabio, Wuhan, China).

Techniques:

Journal: Frontiers in Oncology

Article Title: Enhanced anti−tumor efficacy of “IL−15 and CCL19” −secreting CAR−T cells in human glioblastoma orthotopic xenograft model

doi: 10.3389/fonc.2025.1539055

Figure Lengend Snippet: Generation of EGFRvIII specific CAR-T cells secreting IL-15 and CCL19. (A) Schematic representation of the lentiviral vector construction of EGFRvIII specific CAR secreting IL-15 and CCL19. (B) Flow cytometry analysis depicting the transduction efficiency of lentiviral vectors in transduced human T cells. The expression of EGFRvIII specific CAR was determined using the PE-labeled human EGFRvIII protein. (C) UTD T cells and CAR-T cells were co-cultured with target cells for 24 h. The supernatants from these co-cultures were collected for ELISA to measure the levels of IL-15 (left) and CCL19 (right). Each experiment was repeated independently 3 times, and representative data are shown. Data are the means ± SD of 3 independent experiments, **** P <0.0001.

Article Snippet: The concentrations of IL-15 and CCL19 were measured by ELISA kits (MultiSciences Biotech; NeobioSciences Biotech).

Techniques: Plasmid Preparation, Flow Cytometry, Transduction, Expressing, Labeling, Cell Culture, Enzyme-linked Immunosorbent Assay

Journal: Clinical and Developmental Immunology

Article Title: The Therapeutic Effect of Cytokine-Induced Killer Cells on Pancreatic Cancer Enhanced by Dendritic Cells Pulsed with K-Ras Mutant Peptide

doi: 10.1155/2011/649359

Figure Lengend Snippet: The absorbances of CCL19 and CCL22 at different time points (experiment 2.6). The expression of CCL19 and CCL22 in group K-ras-DCCIK and DCCIK showed uptrend with time and were higher than those of group CIK except for preloading and the 6-hour point. K-ras-DCCIK DCCIK versus CIK after 12 h, * P < 0.01. K-ras-DCCIK versus DCCIK after 12 h, P < 0.05. But the expression in group CIK showed no apparent increase (Figures and ).

Article Snippet: CCL19 and CCL22 ELISA kits were from ADL Inc..

Techniques: Expressing