ccl28  (R&D Systems)

Journal: bioRxiv

Article Title: IgE-producing cells on the move: CCR2 is a key regulator of IgE + plasma cell migration

doi: 10.64898/2025.12.18.695109

Figure Lengend Snippet: (A) Representative histograms showing surface CCR10 expression on IgE + (red) and IgG1 + (blue) gated cells; the filled grey histogram shows the isotype control staining. The accompanying graph shows CCR10 MFI on the gated IgE + and IgG1 + cells. (B) Representative plots of CCR10 expression on IgE + and IgG1 + GC-like B cells, PBs, and PCs. CCR10 MFI across the different IgE + and IgG1 + cell populations from several experiments. (C) The dot plots show the frequency of IgE + and IgG1 + cells after 3h of migration in response to RPMI only or two different concentrations of CCL28, 25nM (300 ng/mL) and 125nM (1.5 μg/mL). (D) CCL28 induced migration shown as a percentage of the IgE + and IgG1 + cells migrating in response to RPMI control. (E) The migration capacity of IgE + and IgG1 + GC-like B cells, plamablasts, and PC in response to CCL28. (F) CCL28 induced migration shown as a percentage of the cells migrating in response to RPMI control. Data are mean + s.d. Statistical analysis was performed using one-way ANOVA with Tukey’s multiple comparison test (B, D, F) or paired two-tailed t -test with Welch’s correction (A); *p< 0.05; **p< 0.01.

Article Snippet: More specifically, we tested the migration of IgE + and IgG1 + cells in response to recombinant human CXCL12 (R&D systems; 300ng/mL), CCL2 (Biolegend; 10ng/mL, 100ng/mL and 300ng/mL) and CCL28 (R&D systems; 300ng/mL and 1.5ug/mL).

Techniques: Expressing, Control, Staining, Migration, Comparison, Two Tailed Test

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: Pericytes recruited by CCL28 promote vascular normalization after anti-angiogenesis therapy through RA/RXRA/ANGPT1 pathway in lung adenocarcinoma

doi: 10.1186/s13046-024-03135-3

Figure Lengend Snippet: CCL28 expression is upregulated after anti-angiogenesis therapy by hypoxia-sensitive transcription factor CEBPB in lung adenocarcinoma

Article Snippet: Briefly, pericytes treated with or without recombinant human CCL28 or CCR3 (R&D Systems, MAB155-100) neutralizing antibodies were collected and fixed by adding a cross-linking agent, formaldehyde, to stabilize the interactions between chromatin proteins and DNA.

Techniques: Expressing

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: Pericytes recruited by CCL28 promote vascular normalization after anti-angiogenesis therapy through RA/RXRA/ANGPT1 pathway in lung adenocarcinoma

doi: 10.1186/s13046-024-03135-3

Figure Lengend Snippet: Tumor-derived CCL28 recruits pericytes to promote vascular normalization in the tumor microenvironment

Article Snippet: Briefly, pericytes treated with or without recombinant human CCL28 or CCR3 (R&D Systems, MAB155-100) neutralizing antibodies were collected and fixed by adding a cross-linking agent, formaldehyde, to stabilize the interactions between chromatin proteins and DNA.

Techniques: Derivative Assay

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: Pericytes recruited by CCL28 promote vascular normalization after anti-angiogenesis therapy through RA/RXRA/ANGPT1 pathway in lung adenocarcinoma

doi: 10.1186/s13046-024-03135-3

Figure Lengend Snippet: Tumor-derived CCL28 promotes the expression of angiopoietin-1 via CCR3 in pericytes

Article Snippet: Briefly, pericytes treated with or without recombinant human CCL28 or CCR3 (R&D Systems, MAB155-100) neutralizing antibodies were collected and fixed by adding a cross-linking agent, formaldehyde, to stabilize the interactions between chromatin proteins and DNA.

Techniques: Derivative Assay, Expressing

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: Pericytes recruited by CCL28 promote vascular normalization after anti-angiogenesis therapy through RA/RXRA/ANGPT1 pathway in lung adenocarcinoma

doi: 10.1186/s13046-024-03135-3

Figure Lengend Snippet: Retinoic acid signaling is activated by CCL28 in pericytes through CCR3 A , Volcano plot of changes in metabolic pathways after CCL28 stimulation. B Volcano plot of the enrichment of gene expression after CCL28 stimulation. C Diagram of the metabolic conversion process in the retinoic acid metabolic signaling pathway. D and E Expression of RDH13 and DHRS11 detected by qPCR and western blot with or without exogenous supplement of CCL28. F Correlation of expression of CCL28 with RDH13 in lung adenocarcinoma. G The protein level of DHRS11 and RDH13 stimulated with or without CCL28 and CCR3 neutralizing antibody in pericytes (left) and gray value was calculated(right). H Knockdown efficiency of RDH13 was confirmed by qPCR. I and J Relative expression of RXRα and ANGPT1 after knockdown of RDH13 with or without stimulation of CCL28. K Representative immunofluorescence images of PAN-CK, NG2, CCL28 with DHRS11 or RDH13 or Angiopoietin-1 on biopsy tissues from lung cancer patients (left panel). Scale bar = 100 μm. The correlation between the expression of CCL28 and the levels of DHRS11, RDH13, and angiopoietin-1 (right panel). Data with error bars are shown as mean ± SEM. Each symbol represents data from a replicate. Each panel is a representative experiment of at least three independent biological replicates. *, **, *** represent p < 0.05, p < 0.01 and p < 0.001, respectively. Abbreviation: MFI, Mean fluorescence intensity

Article Snippet: Briefly, pericytes treated with or without recombinant human CCL28 or CCR3 (R&D Systems, MAB155-100) neutralizing antibodies were collected and fixed by adding a cross-linking agent, formaldehyde, to stabilize the interactions between chromatin proteins and DNA.

Techniques: Gene Expression, Expressing, Western Blot, Knockdown, Immunofluorescence, Fluorescence

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: Pericytes recruited by CCL28 promote vascular normalization after anti-angiogenesis therapy through RA/RXRA/ANGPT1 pathway in lung adenocarcinoma

doi: 10.1186/s13046-024-03135-3

Figure Lengend Snippet: Both CCL28 and retinoic acid could promote vascular normalization in vivo

Article Snippet: Briefly, pericytes treated with or without recombinant human CCL28 or CCR3 (R&D Systems, MAB155-100) neutralizing antibodies were collected and fixed by adding a cross-linking agent, formaldehyde, to stabilize the interactions between chromatin proteins and DNA.

Techniques: In Vivo

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: Pericytes recruited by CCL28 promote vascular normalization after anti-angiogenesis therapy through RA/RXRA/ANGPT1 pathway in lung adenocarcinoma

doi: 10.1186/s13046-024-03135-3

Figure Lengend Snippet: CCL28 is involved in bevacizumab-mediated vascular normalization

Article Snippet: Briefly, pericytes treated with or without recombinant human CCL28 or CCR3 (R&D Systems, MAB155-100) neutralizing antibodies were collected and fixed by adding a cross-linking agent, formaldehyde, to stabilize the interactions between chromatin proteins and DNA.

Techniques:

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: Pericytes recruited by CCL28 promote vascular normalization after anti-angiogenesis therapy through RA/RXRA/ANGPT1 pathway in lung adenocarcinoma

doi: 10.1186/s13046-024-03135-3

Figure Lengend Snippet: A schematic diagram of tumor microenvironment modulation effects of CCL28

Article Snippet: Briefly, pericytes treated with or without recombinant human CCL28 or CCR3 (R&D Systems, MAB155-100) neutralizing antibodies were collected and fixed by adding a cross-linking agent, formaldehyde, to stabilize the interactions between chromatin proteins and DNA.

Techniques:

Journal: Mucosal immunology

Article Title: Th22 cells are efficiently recruited in the gut by CCL28 as an alternative to CCL20 but do not compensate for the loss of Th17 cells in treated HIV-1-infected individuals.

doi: 10.1038/s41385-020-0286-6

Figure Lengend Snippet: Fig. 2 Expression of CCL28 by enterocytes in the duodenal mucosa. CCL28 production in the duodenal mucosa of treated HIV- 1-infected (n = 10) and uninfected individuals (n = 10). Chemokine expression was quantified per surface unit of epithelium using NIS- element (Nikon). CCL28 (red) was stained by immunohistochemistry on an ApoTome (Zeiss, original magnification ×63). Cell nuclei were counterstained (DAPI, blue). Representative treated HIV-1-infected and uninfected individuals are shown. Groups were compared with the Wilcoxon’s rank-sum test. Median bars are shown.

Article Snippet: In gradient experiments, CCL20 and CCL28 recombinant proteins (R&D Systems) were loaded in the bottom chamber with a CCL20/CCL28 ratio varying from 0:100% to 100:100% of their maximum chemotactic activity (10 and 200 ng/mL, respectively).

Techniques: Expressing, Infection, Staining, Immunohistochemistry

Journal: Mucosal immunology

Article Title: Th22 cells are efficiently recruited in the gut by CCL28 as an alternative to CCL20 but do not compensate for the loss of Th17 cells in treated HIV-1-infected individuals.

doi: 10.1038/s41385-020-0286-6

Figure Lengend Snippet: Fig. 3 Impact of the interactions between IL-17A/Th17 cells and IL-22/Th22 cells on CCL20 and CCL28 expression by enterocytes. Effect of IL-17A (white bars) and IL-22 (gray bars) on a CCL20 and b CCL28 mRNA expression by enterocytes. Monolayers of differentiated human primary enterocytes on transwell inserts were stimulated by 0.5, 5, and 50 ng/mL of cytokine. CCL20 and CCL28 mRNA was quantified in the enterocytes by qRT-PCR. CCL20 and CCL28 expression following cytokine stimulation was normalized relatively to the expression in unstimulated epithelial cells (set to 1) and expressed as fold change (log2 scale). Presented data were obtained from at least eight independent experiments performed with different donors. Cuzick’s test for trend was used to compare chemokine expression across the increasing concentrations of cytokines (the corresponding P value is shown on the line above the IL17-A and IL-22 bars); paired Wilcoxon’s test was used to compare chemokine expression upon stimulation vs. unstimulated condition (intradonor pairing); P value is shown above each bar; *P < 0.05; **P < 0.01. Means and SEM are shown. c Effect of Th22:IEC coculture on CCL20 and CCL28 mRNA expression by enterocytes. Enterocytes were cocultured with FACS-sorted Th22 or Th17 cells, added in the bottom chamber for 15 h. CCL20 and CCL28 mRNA were quantified in the enterocytes by qRT-PCR. CCL20 and CCL28 expression in Th22:IEC coculture was normalized relatively to the expression in Th17:IEC coculture (set to 1) and expressed as fold change (log2 scale). Enterocytes production of d CCL20 and e CCL28 proteins in Th22:IEC and Th17:IEC cocultures. CCL20 and CCL28 were quantified in the bottom chamber by ELISA. Presented data were obtained from ten independent experiments performed with different donors. Paired Wilcoxon’s test was used to compare CCL20 and CCL28 in Th22:IEC vs. Th17:IEC cocultures (intradonor pairing); *, P < 0.05. IEC, intestine epithelial cells. Means and SEM are shown.

Article Snippet: In gradient experiments, CCL20 and CCL28 recombinant proteins (R&D Systems) were loaded in the bottom chamber with a CCL20/CCL28 ratio varying from 0:100% to 100:100% of their maximum chemotactic activity (10 and 200 ng/mL, respectively).

Techniques: Expressing, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay

Journal: Frontiers in medicine

Article Title: Activated Hepatic Stellate Cells Induce Infiltration and Formation of CD163 + Macrophages via CCL2/CCR2 Pathway.

doi: 10.3389/fmed.2021.627927

Figure Lengend Snippet: FIGURE 3 | The high level of CCL2 in aHSCs was associated with CD163+ macrophage infiltration and increased with liver fibrosis progression. (A) The primary aHSCs are typically fusiform and express the activation marker α-SMA, together with a high expression of CCL2 protein. (B) The aHSCs secrete high levels of CCL2 (Continued)

Article Snippet: When indicated, recombinant human CCL2 protein (rh CCL2, 2ng/ml, R&D Systems, Abingdon, UK) and INCB 3284 (100ng/ml, Tocris Bioscience, UK) were accordingly added, after which the macrophages were harvested, counted, and analyzed.

Techniques: Activation Assay, Marker, Expressing

Journal: Frontiers in medicine

Article Title: Activated Hepatic Stellate Cells Induce Infiltration and Formation of CD163 + Macrophages via CCL2/CCR2 Pathway.

doi: 10.3389/fmed.2021.627927

Figure Lengend Snippet: FIGURE 4 | CCL2 was responsible for macrophages infiltration and differentiation into M2 phenotype during liver fibrosis. (A) Representative images of macrophage infiltration under different chemotaxis treatments including aHSC, aHSC+INCB, Rh CCL2 and medium. (B) Statistical analysis of the number of macrophages (Continued)

Article Snippet: When indicated, recombinant human CCL2 protein (rh CCL2, 2ng/ml, R&D Systems, Abingdon, UK) and INCB 3284 (100ng/ml, Tocris Bioscience, UK) were accordingly added, after which the macrophages were harvested, counted, and analyzed.

Techniques: Chemotaxis Assay

Journal: The Journal of Clinical Investigation

Article Title: CCL28-induced RAR β expression inhibits oral squamous cell carcinoma bone invasion

doi: 10.1172/JCI125336

Figure Lengend Snippet: (A) Invasion of Ca9.22 and YD10B OSCC cells treated with CCL28 and/or TGF-β (mean ± SEM, n = 3). *P < 0.05 vs. cells without CCL28 and TGF-β; #P < 0.05, ##P < 0.005 vs. TGF-β–only–treated cells by 1-way ANOVA with multiple-comparisons test. (B) Invasion of Ca9.22 and YD10B OSCC cells with CCL28 and/or TGF-β into the CAMs of fertilized eggs (mean ± SEM, n = 3). Representative images of CAM. Scale bars: 100 μm. Cells invaded into the mesoderm layer of CAMs are quantified by the mean fluorescence. *P < 0.05, **P < 0.01 vs. cells without CCL28 and TGF-β; #P < 0.05, ##P < 0.001 vs. TGF-β–only–treated cells by 1-way ANOVA with multiple-comparisons test. (C) Expression levels and cellular localization of E-cadherin and β-catenin in Ca9.22 and YD10B OSCC cells treated with CCL28 and/or TGF-β. Representative immunofluorescence images. Scale bars: 100 μm. (D) Expression levels of E-cadherin, β-catenin, and EMT-regulating transcription factors in Ca9.22 and YD10B OSCC cells treated with CCL28 and/or TGF-β. (E) Cytosolic and nuclear β-catenin levels in Ca9.22 and YD10B OSCC cells treated with CCL28 and/or TGF-β. (D and E) Representative Western blot images.

Article Snippet: Recombinant human CCL28 and TGF-β were obtained from PeproTech.

Techniques: Fluorescence, Expressing, Immunofluorescence, Western Blot

Journal: The Journal of Clinical Investigation

Article Title: CCL28-induced RAR β expression inhibits oral squamous cell carcinoma bone invasion

doi: 10.1172/JCI125336

Figure Lengend Snippet: (A) Invasion of CCL28-knockdown OSCC cells. (B) Invasion of CCR3-knockdown OSCC cells. (C) Invasion of CCR10-knockdown OSCC cells. (A–C) OSCC cells were transduced with lentiviral particles with control shRNAs or 3 different shRNAs targeting CCL28, CCR10, or CCR3. Knockdown of CCL28, CCR10, or CCR3 in transduced cells was confirmed by Western blotting (top panels). Cell invasion is quantified as the number of invaded cells per field (mean ± SEM, n = 3). *P < 0.05, **P < 0.005 vs. control shRNA–transfected cells without CCL28; #P < 0.05, ##P < 0.01 vs. CCL28-, CCR3-, or CCR10-specific shRNA–transfected cells without CCL28 by 1-way ANOVA with multiple-comparisons test. (D) Invasion of CCL28- or CCR10-knockdown OSCC cells labeled with CFDA-SE and then suspended in a DMEM/Matrigel (4:1) mixture on the CAMs of fertilized eggs (mean ± SEM, n = 3). Representative images of CAM. Scale bars: 100 μm. Cells invaded into the mesoderm layer are quantified by the mean fluorescence. *P < 0.05 versus control shRNA–transfected cells without CCL28; #P < 0.01 vs. CCL28- or CCR10-knockdown cells without CCL28 by 1-way ANOVA with multiple-comparisons test. (E) CCL28, CCR3, or CCR10 mRNA levels in normal and HNSCC tissues. The data were obtained from the TCGA database. Box plots show the median and interquartile range. *P < 0.0001 vs. normal tissue by 2-tailed Student’s t test. (F) Kaplan-Meier survival curves for HNSCC patients with high or low expression of CCL28, CCR3, or CCR10 mRNA by the log-rank test.

Article Snippet: Recombinant human CCL28 and TGF-β were obtained from PeproTech.

Techniques: Transduction, Western Blot, shRNA, Transfection, Labeling, Fluorescence, Expressing

Journal: The Journal of Clinical Investigation

Article Title: CCL28-induced RAR β expression inhibits oral squamous cell carcinoma bone invasion

doi: 10.1172/JCI125336

Figure Lengend Snippet: (A) Representative pathway reporter array (n = 2) for wild-type and CCR10-knockdown (KD) OSCC cells in the absence or presence of CCL28 (20 ng/mL). Reporter gene activities in CCL28-treated cells were normalized by those in untreated cells and represented as fold changes. (B) Correlations between CCL28 mRNA expression and RARβ mRNA expression in patients with HNSCC by Pearson’s correlation analysis. Scatter plots represent normalized RSEM values for each gene. (C) RARβ and RARβ2 expression in response to CCL28 treatment (20 pg/mL) in Ca9.22, YD10B, HSC2, or HSC3 OSCC cells. (D) RARβ and RARβ2 expression in CCL28-overexpressing or CCL28-knockdown Ca9.22 or YD10B OSCC cells. (E) RARβ expression in response to CCL28 treatment (20 pg/mL) in CCR3- or CCR10-downregulated Ca9.22 or YD10B OSCC cells. (C–E) Representative Western blot images. (F) Invasion of OSCC cells treated with the RARβ-selective antagonist LE135 or the inverse pan-RAR agonist BMS493 in the presence of CCL28 (20 pg/mL) (mean ± SEM, n = 3). *P < 0.05 and **P < 0.005 versus CCL28-untreated cells; #P < 0.05 and ##P < 0.01 versus CCL28-only-treated cells by 1-way ANOVA with multiple-comparisons test.

Article Snippet: Recombinant human CCL28 and TGF-β were obtained from PeproTech.

Techniques: Expressing, Western Blot

Journal: The Journal of Clinical Investigation

Article Title: CCL28-induced RAR β expression inhibits oral squamous cell carcinoma bone invasion

doi: 10.1172/JCI125336

Figure Lengend Snippet: (A) RARβ and RARβ2 expression levels in OSCC cells treated with CCL28 (20 pg/mL) and/or the selective RARα antagonist ER50891 (ER). (B) Invasion of OSCC cells treated with CCL28 (20 pg/mL) and/or the selective RARα antagonist ER50891 (ER) (mean ± SEM, n = 3). *P < 0.001 versus CCL28-untreated control cells; #P < 0.005 and ##P < 0.001 versus CCL28-only-treated cells by 1-way ANOVA with multiple-comparisons test. (C) Interaction between RARα and HDACs or DNMT in OSCC cells treated with CCL28 (20 pg/mL). Immune complexes were obtained using a Pierce Co-IP kit. (A and C) Representative Western blot images. (D) Acetylated histone H3 levels and HDAC1 interaction at the RARB promoter region of OSCC cells treated with CCL28 (20 pg/mL). Histone modification (H3K9ac) and HDAC1 binding were analyzed by ChIP-qPCR. Data are presented as the percentage of the total chromatin input (% input), and graphs are representative.

Article Snippet: Recombinant human CCL28 and TGF-β were obtained from PeproTech.

Techniques: Expressing, Co-Immunoprecipitation Assay, Western Blot, Modification, Binding Assay

Journal: The Journal of Clinical Investigation

Article Title: CCL28-induced RAR β expression inhibits oral squamous cell carcinoma bone invasion

doi: 10.1172/JCI125336

Figure Lengend Snippet: (A) RANKL and OPG levels secreted by CCL28-treated OSCC cells into the culture media, and the RANKL/OPG ratio (mean ± SEM, n = 3). *P < 0.05 vs. CCL28-untreated cells by 2-tailed Student’s t test. (B) RANKL levels secreted by OSCC cells treated with the selective RARα antagonist ER50891 or the RARβ antagonist LE135 in the presence of CCL28 (mean ± SEM, n = 3). *P < 0.05 versus CCL28-untreated cells; #P < 0.05 versus CCL28-only-treated cells by 1-way ANOVA with multiple comparisons test. (C) RANKL and OPG levels secreted by CCL28-treated osteoblasts into the culture media, and the RANKL/OPG ratio (mean ± SEM, n = 3). *P < 0.05 and **P < 0.01 versus CCL28-untreated cells by 1-way ANOVA with multiple comparisons test. (D) Secreted levels of RANKL and OPG by CCL28-treated osteoblasts in the presence of conditioned media (CM) from OSCC cell lines, and the RANKL/OPG ratio (mean ± SEM, n = 3). #P < 0.05 and ##P < 0.01 versus control cells without CM; *P < 0.05 versus CM-only-treated cells by 1-way ANOVA with multiple-comparisons test. (E) Osteoclast formation in CCL28-treated BMMs in the presence of RANKL (mean ± SEM, n = 3). Representative images at ×100 original magnification. *P < 0.05 versus RANKL-only-treated cells by 1-way ANOVA with multiple comparisons test.

Article Snippet: Recombinant human CCL28 and TGF-β were obtained from PeproTech.

Techniques:

Journal: The Journal of Clinical Investigation

Article Title: CCL28-induced RAR β expression inhibits oral squamous cell carcinoma bone invasion

doi: 10.1172/JCI125336

Figure Lengend Snippet: CCL28 was intraperitoneally administered to mice subcutaneously injected with Ca9.22 OSCC cells in the calvaria (n = 5 for control and n = 10 for experimental groups). (A) Tumor size (mean ± SEM). #P < 0.001 versus vehicle-treated mice by 1-way ANOVA with multiple comparisons test. (B) Representative CT 3D images of calvarial osteolytic lesions. (C) Bone morphometric parameters BV/TV and BS/TV (mean ± SEM). (D) Serum levels of bone turnover markers (mean ± SEM). (E) Representative images of H&E and TRAP staining in calvarial tissue sections. Scale bars: 100 μm. (F) Oc.S/BS determined from TRAP staining as the percentage of bone surface in contact with osteoclasts (mean ± SEM). (C, D, and F) #P < 0.05, ##P < 0.01, and ###P < 0.005 versus control mice; *P < 0.05 and **P < 0.01 versus OSCC cell–injected mice by 1-way ANOVA with multiple comparisons test. (G) Ki67, CD31, and RAR expression levels in calvarial tumor tissues of OSCC-injected mice. Left panel: Representative images of immunohistochemically stained tumor tissues. Scale bars: 100 μm. Graph shows quantified data. *P < 0.05 and **P < 0.01 versus OSCC cell–injected mice by 1-way ANOVA with multiple-comparisons test.

Article Snippet: Recombinant human CCL28 and TGF-β were obtained from PeproTech.

Techniques: Injection, Staining, Expressing

Journal: The Journal of Clinical Investigation

Article Title: CCL28-induced RAR β expression inhibits oral squamous cell carcinoma bone invasion

doi: 10.1172/JCI125336

Figure Lengend Snippet: CCL28 was intraperitoneally administered to mice injected with YD10B OSCC cells into the bone marrow of the right tibia (n = 5 for control and n = 7 for experimental groups). (A) Representative CT 3D images of osteolytic lesions in the tibia. (B) Bone morphometric parameters (mean ± SEM). (C) Serum levels of bone turnover markers (mean ± SEM). (D) Representative images of H&E and TRAP staining in tibial tissue sections. Scale bars: 100 μm. (E) Tumor area determined from H&E staining as the percentage of the total tumor area per tissue area. (F) Oc.S/BS determined from TRAP staining as the percentage of bone surface in contact with osteoclasts (mean ± SEM). (B, C, E, and F) #P < 0.05, ##P < 0.01, and ###P < 0.005 versus control mice; *P < 0.05 and **P < 0.01 versus OSCC cell–injected mice by 1-way ANOVA with multiple comparisons test. (G) Ki67, CD31, and RARβ expression levels in tibial tumor tissues of OSCC-injected mice. Left panel: Representative images of immunohistochemically stained tumor tissues. Scale bars: 100 μm. Right panel: Ki67-positive cells, CD31-positive vessels, and RARβ-positive cells were counted in tumor tissues. *P < 0.05 and **P < 0.01 versus OSCC cell–injected mice by 1-way ANOVA with multiple comparisons test.

Article Snippet: Recombinant human CCL28 and TGF-β were obtained from PeproTech.

Techniques: Injection, Staining, Expressing

Journal: The Journal of Clinical Investigation

Article Title: CCL28-induced RAR β expression inhibits oral squamous cell carcinoma bone invasion

doi: 10.1172/JCI125336

Figure Lengend Snippet: (A) Representative images of IHC staining of CCL28, CCR3, CCR10, and RARβ in normal oral mucosa and OSCC tissues. Scale bars: 100 μm. Magnified images of the boxed area are shown in the insets. Scale bars: 20 μm. (B) Frequency of histoscores in normal oral mucosa and OSCC tissues. (C) Kaplan-Meier survival curve of patients with OSCC stratified based on CCL28, CCR3, CCR10, or RARβ expression by the log-rank test.

Article Snippet: Recombinant human CCL28 and TGF-β were obtained from PeproTech.

Techniques: Immunohistochemistry, Expressing