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R&D Systems goat polyclonal antibodies for cxcl16

Serum cytokine/chemokine array in patients with AP. Serum levels of six chemokines, among 40 cytokines/chemokines investigated, were significantly altered in MAP and SAP patients. Serum levels of CCL21, CCL13, and CCL15 in MAP were significantly lower in patients than in controls. Serum levels of MIF were significantly lower in SAP patients than in MAP patients. Serum levels of CCL27 were significantly lower in SAP patients than in control patients. Serum levels of <t>CXCL16</t> were significantly higher in SAP patients than in control patients. When Bonferroni method was adopted to correct multiple testing problem, only CXCL16 level was revealed to have a significant difference. MAP, mild acute pancreatitis; SAP, severe acute pancreatitis. Results were shown as mean ± SD.

Goat Polyclonal Antibodies For Cxcl16, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 36 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 93 stars, based on 36 article reviews

goat polyclonal antibodies for cxcl16 - by Bioz Stars, 2026-04

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1) Product Images from "Chemokine CXCL16 mediates acinar cell necrosis in cerulein induced acute pancreatitis in mice"

Article Title: Chemokine CXCL16 mediates acinar cell necrosis in cerulein induced acute pancreatitis in mice

Journal: Scientific Reports

doi: 10.1038/s41598-018-27200-y

Figure Legend Snippet: Serum cytokine/chemokine array in patients with AP. Serum levels of six chemokines, among 40 cytokines/chemokines investigated, were significantly altered in MAP and SAP patients. Serum levels of CCL21, CCL13, and CCL15 in MAP were significantly lower in patients than in controls. Serum levels of MIF were significantly lower in SAP patients than in MAP patients. Serum levels of CCL27 were significantly lower in SAP patients than in control patients. Serum levels of CXCL16 were significantly higher in SAP patients than in control patients. When Bonferroni method was adopted to correct multiple testing problem, only CXCL16 level was revealed to have a significant difference. MAP, mild acute pancreatitis; SAP, severe acute pancreatitis. Results were shown as mean ± SD.

Techniques Used:

Cxcl16 expression in acute necrotizing pancreatitis. ( A ) Protocols of acute necrotizing pancreatitis by repeated injection of cerulein. Cerulein (100 ug/kg) was injected every 1 h 8 times on 2 consecutive days into C57BL/6 mice. Four to five mice were sacrificed at the indicated time points. ( B ) Serum amylase level and ( C ) pathology score of the respective time-points. ( D ) H&E sections in the pancreas of mice treated with acute necrotizing pancreatitis regimen at 0, 9, 24, and 33 h, respectively. The section at 33 h shows disrupted acinar architecture, vacuolization and necrosis of acinar cells, and inflammatory cell infiltration. ( E ) Pancreatic mRNA expressions of Cxcl16 , Tnfα , Il6 , and Cxcl2 were determined by quantitative RT-PCR analysis. *p < 0.05 Results were shown as mean ± SD.

Figure Legend Snippet: Cxcl16 expression in acute necrotizing pancreatitis. ( A ) Protocols of acute necrotizing pancreatitis by repeated injection of cerulein. Cerulein (100 ug/kg) was injected every 1 h 8 times on 2 consecutive days into C57BL/6 mice. Four to five mice were sacrificed at the indicated time points. ( B ) Serum amylase level and ( C ) pathology score of the respective time-points. ( D ) H&E sections in the pancreas of mice treated with acute necrotizing pancreatitis regimen at 0, 9, 24, and 33 h, respectively. The section at 33 h shows disrupted acinar architecture, vacuolization and necrosis of acinar cells, and inflammatory cell infiltration. ( E ) Pancreatic mRNA expressions of Cxcl16 , Tnfα , Il6 , and Cxcl2 were determined by quantitative RT-PCR analysis. *p < 0.05 Results were shown as mean ± SD.

Techniques Used: Expressing, Injection, Quantitative RT-PCR

Cxcl16 −/− mice were resistant to the development of necrotizing pancreatitis. Cerulein (100 ug/kg) was injected into Cxcl16 -intact ( WT ) and Cxcl16 -deficient ( Cxcl16 −/− ) mice (n = 5 in each group) every 1 h 8 times on 2 consecutive days as decribed in Fig. ( A ) Serum amylase levels and ( B ) pathology scores of WT and Cxcl16 −/− mice. ( C ) H&E sections from WT and Cxcl16 −/− mice at 24 h and 33 h. ( D ) Immunostained (Gr1, F4/80, and CD3) sections from WT and Cxcl16 −/− mice at 33 h. ( E ) Semiquantitative assessment of infiltartion of neutrophils, macrophages, and T cells. The number of neutrophils, macrophages, and T cells were counted in 5 high powered fields in each pancreas sections of WT and Cxcl16 −/− mice at 33 h. ( F ) MPO levels determined by ELISA in the pancreatic lysates of WT and Cxcl16 −/− mice at 33 h. *p < 0.05 Results were shown as mean ± SD.

Figure Legend Snippet: Cxcl16 −/− mice were resistant to the development of necrotizing pancreatitis. Cerulein (100 ug/kg) was injected into Cxcl16 -intact ( WT ) and Cxcl16 -deficient ( Cxcl16 −/− ) mice (n = 5 in each group) every 1 h 8 times on 2 consecutive days as decribed in Fig. ( A ) Serum amylase levels and ( B ) pathology scores of WT and Cxcl16 −/− mice. ( C ) H&E sections from WT and Cxcl16 −/− mice at 24 h and 33 h. ( D ) Immunostained (Gr1, F4/80, and CD3) sections from WT and Cxcl16 −/− mice at 33 h. ( E ) Semiquantitative assessment of infiltartion of neutrophils, macrophages, and T cells. The number of neutrophils, macrophages, and T cells were counted in 5 high powered fields in each pancreas sections of WT and Cxcl16 −/− mice at 33 h. ( F ) MPO levels determined by ELISA in the pancreatic lysates of WT and Cxcl16 −/− mice at 33 h. *p < 0.05 Results were shown as mean ± SD.

Techniques Used: Injection, Enzyme-linked Immunosorbent Assay

Acinar cell expression of Cxcl16. Cerulein (100 µg/kg) was injected into WT and Cxcl16 −/− mice every 1 h 8 times on 2 consecutive days as described in Fig. . ( A ) Cxcl16 immunostaining of pancreatic frozen sections from WT mice (0 and 33 h) and Cxcl16 −/− mouse (33 h). ( B ) Dual immunofluorescence of Cxcl16 (Alexa Fluor 488) and amylase (Alexa Fluor 594), or Cxcl16 (Alexa Fluor 594) and F4/80 (Alexa Fluor 488). Most of Cxcl16-expressing on the cell surface was positive for cytoplasmic amylase expression. ( C ) Macrophage-depleted AP model (Left, protocol). Clodronate liposomes (100 mg/kg) were injected at 24 h before the first cerulein injection. F4/80 and Cxcl16 mRNA expression in the pancreas at 33 h, relative to those of control mice at 0 h, was evaluated at 33 h. *p < 0.05 Results were shown as mean ± SD.

Figure Legend Snippet: Acinar cell expression of Cxcl16. Cerulein (100 µg/kg) was injected into WT and Cxcl16 −/− mice every 1 h 8 times on 2 consecutive days as described in Fig. . ( A ) Cxcl16 immunostaining of pancreatic frozen sections from WT mice (0 and 33 h) and Cxcl16 −/− mouse (33 h). ( B ) Dual immunofluorescence of Cxcl16 (Alexa Fluor 488) and amylase (Alexa Fluor 594), or Cxcl16 (Alexa Fluor 594) and F4/80 (Alexa Fluor 488). Most of Cxcl16-expressing on the cell surface was positive for cytoplasmic amylase expression. ( C ) Macrophage-depleted AP model (Left, protocol). Clodronate liposomes (100 mg/kg) were injected at 24 h before the first cerulein injection. F4/80 and Cxcl16 mRNA expression in the pancreas at 33 h, relative to those of control mice at 0 h, was evaluated at 33 h. *p < 0.05 Results were shown as mean ± SD.

Techniques Used: Expressing, Injection, Immunostaining, Immunofluorescence, Liposomes

Induction of Ccl9 by Cxcl16 in necrotizing acute pancreatitis. ( A ) Cytokine/chemokine array using pancreatic lysates from C57BL/6 mice and Cxcl16 −/− mice treated with necrotizing pancreatitis regimen as described in Fig. . The relative expression of cytokines and chemokines is shown together with representative images. The data presented were obtained from WT and Cxcl16 −/− mice at 33 h, and WT on 0 h. ( B ) Ccl9 , Vcam-1 , and Ccl2 mRNA expression, relative to those of WT mice at 0 h, was assessed by qPCR in the pancreas of WT and Cxcl16 −/− mice at 33 h. ( C ) Ccl9 immunostaining of pancreatic frozen sections from WT mice at 0 h and 33 h, and Cxcl16 −/− mice at 33 h. *p < 0.05 Results were shown as mean ± SD.

Figure Legend Snippet: Induction of Ccl9 by Cxcl16 in necrotizing acute pancreatitis. ( A ) Cytokine/chemokine array using pancreatic lysates from C57BL/6 mice and Cxcl16 −/− mice treated with necrotizing pancreatitis regimen as described in Fig. . The relative expression of cytokines and chemokines is shown together with representative images. The data presented were obtained from WT and Cxcl16 −/− mice at 33 h, and WT on 0 h. ( B ) Ccl9 , Vcam-1 , and Ccl2 mRNA expression, relative to those of WT mice at 0 h, was assessed by qPCR in the pancreas of WT and Cxcl16 −/− mice at 33 h. ( C ) Ccl9 immunostaining of pancreatic frozen sections from WT mice at 0 h and 33 h, and Cxcl16 −/− mice at 33 h. *p < 0.05 Results were shown as mean ± SD.

Techniques Used: Expressing, Immunostaining

Expression of Ccl9 by pancreatic acinar cells. ( A ) Amylase secretion by the rat acinar cell line AR42J upon stimulation with various concentrations of cerulein. ( B ) Cxcl16 and Ccl9 mRNA expression by AR42J upon stimulation with cerulein. ( C ) Ccl9 mRNA expression of AR42J upon stimulation with cerulein (10 −10 M) in combination with various concentrations of recombinant Cxcl16 protein (left). Ccl9 mRNA expression of AR42J upon stimulation with cerulein (10 −7 M) in the presence of neutralizing anti-Cxcl16 Ab or control Ab (right). ( D ) Cxcl16 and Ccl9 mRNA expression by pancreatic acinar cells isolated from WT and Cxcl16 −/− mice upon stimulation with cerulein (10 −7 M). *p < 0.05 Results were shown as mean ± SD.

Figure Legend Snippet: Expression of Ccl9 by pancreatic acinar cells. ( A ) Amylase secretion by the rat acinar cell line AR42J upon stimulation with various concentrations of cerulein. ( B ) Cxcl16 and Ccl9 mRNA expression by AR42J upon stimulation with cerulein. ( C ) Ccl9 mRNA expression of AR42J upon stimulation with cerulein (10 −10 M) in combination with various concentrations of recombinant Cxcl16 protein (left). Ccl9 mRNA expression of AR42J upon stimulation with cerulein (10 −7 M) in the presence of neutralizing anti-Cxcl16 Ab or control Ab (right). ( D ) Cxcl16 and Ccl9 mRNA expression by pancreatic acinar cells isolated from WT and Cxcl16 −/− mice upon stimulation with cerulein (10 −7 M). *p < 0.05 Results were shown as mean ± SD.

Techniques Used: Expressing, Recombinant, Isolation

Therapeutic effects of neutralizing Cxcl16 Ab in the necrotizing pancreatitis model. ( A ) Injection protocol of anti-Cxcl16 Ab in necrotizing pancreatitis model. ( B ) Serum amylase level, ( C ) representative H&E sections, and pathology score of control Ab or anti-Cxcl16 Ab-treated mice at 39 h. ( D ) Gr1 immunostained sections and neutrophil counts of control Ab or anti-Cxcl16 Ab-treated mice at 39 h. ( E ) Pancreatic Ccl9 mRNA, pancreatic Ccl9 protein, and serum Ccl9 protein levels in control Ab or anti-Cxcl16 Ab-treated mice at 39 h. n = 5 in each group. *p < 0.05 Results were shown as mean ± SD.

Figure Legend Snippet: Therapeutic effects of neutralizing Cxcl16 Ab in the necrotizing pancreatitis model. ( A ) Injection protocol of anti-Cxcl16 Ab in necrotizing pancreatitis model. ( B ) Serum amylase level, ( C ) representative H&E sections, and pathology score of control Ab or anti-Cxcl16 Ab-treated mice at 39 h. ( D ) Gr1 immunostained sections and neutrophil counts of control Ab or anti-Cxcl16 Ab-treated mice at 39 h. ( E ) Pancreatic Ccl9 mRNA, pancreatic Ccl9 protein, and serum Ccl9 protein levels in control Ab or anti-Cxcl16 Ab-treated mice at 39 h. n = 5 in each group. *p < 0.05 Results were shown as mean ± SD.

Techniques Used: Injection

Image Search Results

Journal: Scientific Reports

Article Title: Chemokine CXCL16 mediates acinar cell necrosis in cerulein induced acute pancreatitis in mice

doi: 10.1038/s41598-018-27200-y

Figure Lengend Snippet: Serum cytokine/chemokine array in patients with AP. Serum levels of six chemokines, among 40 cytokines/chemokines investigated, were significantly altered in MAP and SAP patients. Serum levels of CCL21, CCL13, and CCL15 in MAP were significantly lower in patients than in controls. Serum levels of MIF were significantly lower in SAP patients than in MAP patients. Serum levels of CCL27 were significantly lower in SAP patients than in control patients. Serum levels of CXCL16 were significantly higher in SAP patients than in control patients. When Bonferroni method was adopted to correct multiple testing problem, only CXCL16 level was revealed to have a significant difference. MAP, mild acute pancreatitis; SAP, severe acute pancreatitis. Results were shown as mean ± SD.

Article Snippet: The sections were fixed with ice-cold methanol and immunostained using the following primary antibodies: goat polyclonal antibodies for Cxcl16 (R&D Systems, Minneapolis, MN) and Ccl9 (R&D Systems), a rabbit polyclonal antibody for amylase (Sigma-Aldrich).

Techniques:

Journal: Scientific Reports

Article Title: Chemokine CXCL16 mediates acinar cell necrosis in cerulein induced acute pancreatitis in mice

doi: 10.1038/s41598-018-27200-y

Figure Lengend Snippet: Cxcl16 expression in acute necrotizing pancreatitis. ( A ) Protocols of acute necrotizing pancreatitis by repeated injection of cerulein. Cerulein (100 ug/kg) was injected every 1 h 8 times on 2 consecutive days into C57BL/6 mice. Four to five mice were sacrificed at the indicated time points. ( B ) Serum amylase level and ( C ) pathology score of the respective time-points. ( D ) H&E sections in the pancreas of mice treated with acute necrotizing pancreatitis regimen at 0, 9, 24, and 33 h, respectively. The section at 33 h shows disrupted acinar architecture, vacuolization and necrosis of acinar cells, and inflammatory cell infiltration. ( E ) Pancreatic mRNA expressions of Cxcl16 , Tnfα , Il6 , and Cxcl2 were determined by quantitative RT-PCR analysis. *p < 0.05 Results were shown as mean ± SD.

Techniques: Expressing, Injection, Quantitative RT-PCR

Journal: Scientific Reports

Article Title: Chemokine CXCL16 mediates acinar cell necrosis in cerulein induced acute pancreatitis in mice

doi: 10.1038/s41598-018-27200-y

Figure Lengend Snippet: Cxcl16 −/− mice were resistant to the development of necrotizing pancreatitis. Cerulein (100 ug/kg) was injected into Cxcl16 -intact ( WT ) and Cxcl16 -deficient ( Cxcl16 −/− ) mice (n = 5 in each group) every 1 h 8 times on 2 consecutive days as decribed in Fig. ( A ) Serum amylase levels and ( B ) pathology scores of WT and Cxcl16 −/− mice. ( C ) H&E sections from WT and Cxcl16 −/− mice at 24 h and 33 h. ( D ) Immunostained (Gr1, F4/80, and CD3) sections from WT and Cxcl16 −/− mice at 33 h. ( E ) Semiquantitative assessment of infiltartion of neutrophils, macrophages, and T cells. The number of neutrophils, macrophages, and T cells were counted in 5 high powered fields in each pancreas sections of WT and Cxcl16 −/− mice at 33 h. ( F ) MPO levels determined by ELISA in the pancreatic lysates of WT and Cxcl16 −/− mice at 33 h. *p < 0.05 Results were shown as mean ± SD.

Techniques: Injection, Enzyme-linked Immunosorbent Assay

Journal: Scientific Reports

Article Title: Chemokine CXCL16 mediates acinar cell necrosis in cerulein induced acute pancreatitis in mice

doi: 10.1038/s41598-018-27200-y

Figure Lengend Snippet: Acinar cell expression of Cxcl16. Cerulein (100 µg/kg) was injected into WT and Cxcl16 −/− mice every 1 h 8 times on 2 consecutive days as described in Fig. . ( A ) Cxcl16 immunostaining of pancreatic frozen sections from WT mice (0 and 33 h) and Cxcl16 −/− mouse (33 h). ( B ) Dual immunofluorescence of Cxcl16 (Alexa Fluor 488) and amylase (Alexa Fluor 594), or Cxcl16 (Alexa Fluor 594) and F4/80 (Alexa Fluor 488). Most of Cxcl16-expressing on the cell surface was positive for cytoplasmic amylase expression. ( C ) Macrophage-depleted AP model (Left, protocol). Clodronate liposomes (100 mg/kg) were injected at 24 h before the first cerulein injection. F4/80 and Cxcl16 mRNA expression in the pancreas at 33 h, relative to those of control mice at 0 h, was evaluated at 33 h. *p < 0.05 Results were shown as mean ± SD.

Techniques: Expressing, Injection, Immunostaining, Immunofluorescence, Liposomes

Journal: Scientific Reports

Article Title: Chemokine CXCL16 mediates acinar cell necrosis in cerulein induced acute pancreatitis in mice

doi: 10.1038/s41598-018-27200-y

Figure Lengend Snippet: Induction of Ccl9 by Cxcl16 in necrotizing acute pancreatitis. ( A ) Cytokine/chemokine array using pancreatic lysates from C57BL/6 mice and Cxcl16 −/− mice treated with necrotizing pancreatitis regimen as described in Fig. . The relative expression of cytokines and chemokines is shown together with representative images. The data presented were obtained from WT and Cxcl16 −/− mice at 33 h, and WT on 0 h. ( B ) Ccl9 , Vcam-1 , and Ccl2 mRNA expression, relative to those of WT mice at 0 h, was assessed by qPCR in the pancreas of WT and Cxcl16 −/− mice at 33 h. ( C ) Ccl9 immunostaining of pancreatic frozen sections from WT mice at 0 h and 33 h, and Cxcl16 −/− mice at 33 h. *p < 0.05 Results were shown as mean ± SD.

Techniques: Expressing, Immunostaining

Journal: Scientific Reports

Article Title: Chemokine CXCL16 mediates acinar cell necrosis in cerulein induced acute pancreatitis in mice

doi: 10.1038/s41598-018-27200-y

Figure Lengend Snippet: Expression of Ccl9 by pancreatic acinar cells. ( A ) Amylase secretion by the rat acinar cell line AR42J upon stimulation with various concentrations of cerulein. ( B ) Cxcl16 and Ccl9 mRNA expression by AR42J upon stimulation with cerulein. ( C ) Ccl9 mRNA expression of AR42J upon stimulation with cerulein (10 −10 M) in combination with various concentrations of recombinant Cxcl16 protein (left). Ccl9 mRNA expression of AR42J upon stimulation with cerulein (10 −7 M) in the presence of neutralizing anti-Cxcl16 Ab or control Ab (right). ( D ) Cxcl16 and Ccl9 mRNA expression by pancreatic acinar cells isolated from WT and Cxcl16 −/− mice upon stimulation with cerulein (10 −7 M). *p < 0.05 Results were shown as mean ± SD.

Techniques: Expressing, Recombinant, Isolation

Journal: Scientific Reports

Article Title: Chemokine CXCL16 mediates acinar cell necrosis in cerulein induced acute pancreatitis in mice

doi: 10.1038/s41598-018-27200-y

Figure Lengend Snippet: Therapeutic effects of neutralizing Cxcl16 Ab in the necrotizing pancreatitis model. ( A ) Injection protocol of anti-Cxcl16 Ab in necrotizing pancreatitis model. ( B ) Serum amylase level, ( C ) representative H&E sections, and pathology score of control Ab or anti-Cxcl16 Ab-treated mice at 39 h. ( D ) Gr1 immunostained sections and neutrophil counts of control Ab or anti-Cxcl16 Ab-treated mice at 39 h. ( E ) Pancreatic Ccl9 mRNA, pancreatic Ccl9 protein, and serum Ccl9 protein levels in control Ab or anti-Cxcl16 Ab-treated mice at 39 h. n = 5 in each group. *p < 0.05 Results were shown as mean ± SD.

Techniques: Injection

Metalloproteinase inhibitor GM-6001 enhances cytokine production induced by D-ODN. (a) PBMC (4 × 10 6 /mL) were preincubated in the absence or presence of GM6001 (50 μ M) for 30 min, fixed, and stained for CXCL16 expression. Cells treated as in (a) were washed and then stimulated with 3 μ M D-ODN (b), 1 μ M of C ODN (c), or 1 μ M of K-ODN (d) for 24 h. Cytokine production (IL-6 for K-ODN and IFN α for D and C ODN) was assessed from culture supernatants using ELISA. Response of 6 individual donors is shown.

Journal: Mediators of Inflammation

Article Title: Plasmacytoid Dendritic Cell Response to CpG ODN Correlates with CXCL16 Expression and Is Inhibited by ox-LDL

doi: 10.1155/2013/312590

Figure Lengend Snippet: Metalloproteinase inhibitor GM-6001 enhances cytokine production induced by D-ODN. (a) PBMC (4 × 10 6 /mL) were preincubated in the absence or presence of GM6001 (50 μ M) for 30 min, fixed, and stained for CXCL16 expression. Cells treated as in (a) were washed and then stimulated with 3 μ M D-ODN (b), 1 μ M of C ODN (c), or 1 μ M of K-ODN (d) for 24 h. Cytokine production (IL-6 for K-ODN and IFN α for D and C ODN) was assessed from culture supernatants using ELISA. Response of 6 individual donors is shown.

Article Snippet: Polyclonal goat anti-human CXCL16 (purified and biotin labeled) and its isotype matched control were from R&D Systems.

Techniques: Staining, Expressing, Enzyme-linked Immunosorbent Assay

Altering CXCL16 expression influences “D” ODN induced cytokine production.

Journal: Mediators of Inflammation

Article Title: Plasmacytoid Dendritic Cell Response to CpG ODN Correlates with CXCL16 Expression and Is Inhibited by ox-LDL

doi: 10.1155/2013/312590

Figure Lengend Snippet: Altering CXCL16 expression influences “D” ODN induced cytokine production.

Article Snippet: Polyclonal goat anti-human CXCL16 (purified and biotin labeled) and its isotype matched control were from R&D Systems.

Techniques: Expressing

Digestion of CXCL16 on the surface of pDCs reduces cytokine production induced by D-ODN. (a) PBMC (4 × 10 6 /mL) were preincubated in the absence or presence of O-sialoglycoprotein endopeptidase (25 μ g/mL) for 30 min, fixed, and stained for CXCL16 expression. (b) Cells treated as in (a) were washed and then stimulated with 3 μ M D-ODN for 24 h. Cytokine production was assessed from culture supernatants using ELISA. Response of 6 individual donors is shown.

Journal: Mediators of Inflammation

Article Title: Plasmacytoid Dendritic Cell Response to CpG ODN Correlates with CXCL16 Expression and Is Inhibited by ox-LDL

doi: 10.1155/2013/312590

Figure Lengend Snippet: Digestion of CXCL16 on the surface of pDCs reduces cytokine production induced by D-ODN. (a) PBMC (4 × 10 6 /mL) were preincubated in the absence or presence of O-sialoglycoprotein endopeptidase (25 μ g/mL) for 30 min, fixed, and stained for CXCL16 expression. (b) Cells treated as in (a) were washed and then stimulated with 3 μ M D-ODN for 24 h. Cytokine production was assessed from culture supernatants using ELISA. Response of 6 individual donors is shown.

Article Snippet: Polyclonal goat anti-human CXCL16 (purified and biotin labeled) and its isotype matched control were from R&D Systems.

Techniques: Staining, Expressing, Enzyme-linked Immunosorbent Assay

CXCL16/CXCR6 interaction reduces the threshold of activation in pDCs responding to D-ODN. (a) pDCs were enriched from human PBMCs using the BDCA-4 isolation kit as recommended by the manufacturer. Purity of cells was established by flow cytometry following staining with pDC associated cell-surface markers. (b) Enriched pDCs (100,000 cells/well) were incubated with CXCR6 or CCR5 expressing Jurkat T cells (1 : 1 ratio) in 96-well U-bottom plates. Cocultures were then stimulated with a suboptimal concentration of D-ODN (0.75 μ g/mL). pDC stimulated with optimal concentration of D-ODN (10 μ g/mL) served as a positive control. Cytokine production was assessed from culture supernatants 24 h later using ELISA. Average response of 3 different pDC preparations is shown (mean ± S.D).

Journal: Mediators of Inflammation

Article Title: Plasmacytoid Dendritic Cell Response to CpG ODN Correlates with CXCL16 Expression and Is Inhibited by ox-LDL

doi: 10.1155/2013/312590

Figure Lengend Snippet: CXCL16/CXCR6 interaction reduces the threshold of activation in pDCs responding to D-ODN. (a) pDCs were enriched from human PBMCs using the BDCA-4 isolation kit as recommended by the manufacturer. Purity of cells was established by flow cytometry following staining with pDC associated cell-surface markers. (b) Enriched pDCs (100,000 cells/well) were incubated with CXCR6 or CCR5 expressing Jurkat T cells (1 : 1 ratio) in 96-well U-bottom plates. Cocultures were then stimulated with a suboptimal concentration of D-ODN (0.75 μ g/mL). pDC stimulated with optimal concentration of D-ODN (10 μ g/mL) served as a positive control. Cytokine production was assessed from culture supernatants 24 h later using ELISA. Average response of 3 different pDC preparations is shown (mean ± S.D).

Article Snippet: Polyclonal goat anti-human CXCL16 (purified and biotin labeled) and its isotype matched control were from R&D Systems.

Techniques: Activation Assay, Isolation, Flow Cytometry, Staining, Incubation, Expressing, Concentration Assay, Positive Control, Enzyme-linked Immunosorbent Assay

Oxidized LDL and recombinant IFN γ /TNF α modify cytokine production induced by D-ODN. (a) Enriched pDCs (100,000 cells/well) were preincubated with LDL or OxLDL (10 μ g/mL each) and then stimulated with 3 μ M of D-ODN. Cytokine production was assessed from culture supernatants 24 h later using ELISA. Average response of 3 different pDC preparations is shown (mean ± S.D). (b) Enriched pDCs were preincubated in the absence or presence of GM6001 (50 μ M), recIFN γ /TNF α (20 ng/mL each), or PMA/ionomycin (250 pg/mL/100 pg/mL) for 30 min at 37°C. Cytokine production was assessed from culture supernatants 24 h later using ELISA. Average response of 3 different pDC preparations is shown (mean ± S.D). (c) PBMC (4 × 10 6 /mL) were preincubated in the absence or presence of 1 μ M Control ODN, 1 μ M K-ODN, or 3 μ M D-ODN for 48 h. Cells were then fixed and stained for CXCL16 expression. MFI of CXCL16 stained cells ± S.D of 3 different donors is shown.

Journal: Mediators of Inflammation

Article Title: Plasmacytoid Dendritic Cell Response to CpG ODN Correlates with CXCL16 Expression and Is Inhibited by ox-LDL

doi: 10.1155/2013/312590

Figure Lengend Snippet: Oxidized LDL and recombinant IFN γ /TNF α modify cytokine production induced by D-ODN. (a) Enriched pDCs (100,000 cells/well) were preincubated with LDL or OxLDL (10 μ g/mL each) and then stimulated with 3 μ M of D-ODN. Cytokine production was assessed from culture supernatants 24 h later using ELISA. Average response of 3 different pDC preparations is shown (mean ± S.D). (b) Enriched pDCs were preincubated in the absence or presence of GM6001 (50 μ M), recIFN γ /TNF α (20 ng/mL each), or PMA/ionomycin (250 pg/mL/100 pg/mL) for 30 min at 37°C. Cytokine production was assessed from culture supernatants 24 h later using ELISA. Average response of 3 different pDC preparations is shown (mean ± S.D). (c) PBMC (4 × 10 6 /mL) were preincubated in the absence or presence of 1 μ M Control ODN, 1 μ M K-ODN, or 3 μ M D-ODN for 48 h. Cells were then fixed and stained for CXCL16 expression. MFI of CXCL16 stained cells ± S.D of 3 different donors is shown.

Article Snippet: Polyclonal goat anti-human CXCL16 (purified and biotin labeled) and its isotype matched control were from R&D Systems.

Techniques: Recombinant, Enzyme-linked Immunosorbent Assay, Control, Staining, Expressing

( A, B ) mRNA expression of CXCL16 ( A ) and CXCR6 ( B ) was evaluated by Q-PCR. The expression of CXCL16 and CXCR6 is higher in colonic mucosa of patients with Crohn’s disease (CD) compared with patients with ulcerative colitis (UC) and healthy controls. Data were normalized to expression of GAPDH mRNA. ( n = 5–10; mean and s.e.m.). *, P < 0.05. ( C ) Correlation between CXCL16 and CXCR6 mRNA expression in the colonic mucosa of CD patients. Statistical analysis was performed by Spearman’s correlation; correlation coefficient = 0.76, P = 0.024. ( D, E ) Immunohistochemistry of CXCL16 ( D ) and CXCL16 ( E ) was performed on colonic mucosa of patients with CD and healthy controls. CXCL16 positive staining was observed on epithelial cells and a subset of colonic LP cells in CD patients ( D ). CXCR6 was strongly expressed by small round cells in CD mucosa ( E ). Scale bars, 50 µm, IgG indicates a control antibody. Representative photomicrographs obtained from the analysis of five or six specimens per group are shown.

Journal: PLoS ONE

Article Title: Distinct Roles for CXCR6 + and CXCR6 − CD4 + T Cells in the Pathogenesis of Chronic Colitis

doi: 10.1371/journal.pone.0065488

Figure Lengend Snippet: ( A, B ) mRNA expression of CXCL16 ( A ) and CXCR6 ( B ) was evaluated by Q-PCR. The expression of CXCL16 and CXCR6 is higher in colonic mucosa of patients with Crohn’s disease (CD) compared with patients with ulcerative colitis (UC) and healthy controls. Data were normalized to expression of GAPDH mRNA. ( n = 5–10; mean and s.e.m.). *, P < 0.05. ( C ) Correlation between CXCL16 and CXCR6 mRNA expression in the colonic mucosa of CD patients. Statistical analysis was performed by Spearman’s correlation; correlation coefficient = 0.76, P = 0.024. ( D, E ) Immunohistochemistry of CXCL16 ( D ) and CXCL16 ( E ) was performed on colonic mucosa of patients with CD and healthy controls. CXCL16 positive staining was observed on epithelial cells and a subset of colonic LP cells in CD patients ( D ). CXCR6 was strongly expressed by small round cells in CD mucosa ( E ). Scale bars, 50 µm, IgG indicates a control antibody. Representative photomicrographs obtained from the analysis of five or six specimens per group are shown.

Article Snippet: The sections were incubated with 5% bovine serum albumin in PBS for 30 min at room temperature and then with goat anti-human CXCL16 polyclonal Ab (R&D Systems), mouse anti-human CXCR6 monoclonal Ab (R&D Systems), or an identical concentration of control goat or mouse IgG, overnight at 4°C.

Techniques: Expressing, Immunohistochemistry, Staining

( A ) Cxcl16 mRNA levels in colonic epithelium (CEC) and distal colon tissues were analyzed by Q-PCR 8 weeks after transfer. The expression of Cxcl16 mRNA increased in both epithelium and colon tissues of the transfer model compared with healthy Rag1 −/− mice. Data were normalized to expression of Gapdh mRNA. ( n = 5; mean and s.d.). **, P < 0.01. ( B ) CXCL16 immunostaining of the distal colon in colitic and healthy Rag1 −/− mice. Scale bars, 100 µm. Data are representative of two independent experiments. ( C ) CXCR6 expression on CD4 + T cells was analyzed by flow cytometry using a mouse CXCL16-human IgG-Fc fusion protein or control human IgG-Fcγ at 8-week post transfer. CXCR6 was expressed at high levels by the majority of colonic LP CD4 + T cells in the colitic mice, by about half of the SP and MLN CD4 + T cells, and by ∼20% of BM cells. ( D ) Absolute numbers of CXCR6 + and CXCR6 − CD4 + T cells in each of tissues were calculated based on the flow cytometric analysis described in ( C ). Data are representative of three independent experiments (mean and s.d.). **, P < 0.01.

Journal: PLoS ONE

Article Title: Distinct Roles for CXCR6 + and CXCR6 − CD4 + T Cells in the Pathogenesis of Chronic Colitis

doi: 10.1371/journal.pone.0065488

Figure Lengend Snippet: ( A ) Cxcl16 mRNA levels in colonic epithelium (CEC) and distal colon tissues were analyzed by Q-PCR 8 weeks after transfer. The expression of Cxcl16 mRNA increased in both epithelium and colon tissues of the transfer model compared with healthy Rag1 −/− mice. Data were normalized to expression of Gapdh mRNA. ( n = 5; mean and s.d.). **, P < 0.01. ( B ) CXCL16 immunostaining of the distal colon in colitic and healthy Rag1 −/− mice. Scale bars, 100 µm. Data are representative of two independent experiments. ( C ) CXCR6 expression on CD4 + T cells was analyzed by flow cytometry using a mouse CXCL16-human IgG-Fc fusion protein or control human IgG-Fcγ at 8-week post transfer. CXCR6 was expressed at high levels by the majority of colonic LP CD4 + T cells in the colitic mice, by about half of the SP and MLN CD4 + T cells, and by ∼20% of BM cells. ( D ) Absolute numbers of CXCR6 + and CXCR6 − CD4 + T cells in each of tissues were calculated based on the flow cytometric analysis described in ( C ). Data are representative of three independent experiments (mean and s.d.). **, P < 0.01.

Techniques: Expressing, Immunostaining, Flow Cytometry

( A ) Body weight of Rag1 −/− recipients of i.v. injected purified CD45RB high CD4 + T cells form Cxcr6 +/Egfp or Cxcr6 Egfp/Egfp (CXCR6-deficient) mice on day 0, presented as percent of original weight. ( B ) Colon weight of the mice in ( A ) on week 7. Data are representative of two independent experiments (mean and s.d.). ( C ) Histology of colon tissues from the mice in B . ( D ) CXCR6 expression by LP CD4 + T cells was analyzed by flow cytometry using CXCL16-hFc at 7-week post transfer. ( E ) Expression levels of indicated cytokines in distal colon were analyzed by Q-PCR at 7 weeks after the transfer. Data were normalized to expression of Gapdh . ( n = 4 or 5; mean and s.d.).

Journal: PLoS ONE

Article Title: Distinct Roles for CXCR6 + and CXCR6 − CD4 + T Cells in the Pathogenesis of Chronic Colitis

doi: 10.1371/journal.pone.0065488

Figure Lengend Snippet: ( A ) Body weight of Rag1 −/− recipients of i.v. injected purified CD45RB high CD4 + T cells form Cxcr6 +/Egfp or Cxcr6 Egfp/Egfp (CXCR6-deficient) mice on day 0, presented as percent of original weight. ( B ) Colon weight of the mice in ( A ) on week 7. Data are representative of two independent experiments (mean and s.d.). ( C ) Histology of colon tissues from the mice in B . ( D ) CXCR6 expression by LP CD4 + T cells was analyzed by flow cytometry using CXCL16-hFc at 7-week post transfer. ( E ) Expression levels of indicated cytokines in distal colon were analyzed by Q-PCR at 7 weeks after the transfer. Data were normalized to expression of Gapdh . ( n = 4 or 5; mean and s.d.).

Techniques: Injection, Purification, Expressing, Flow Cytometry

( A ) Schematic transfer protocol. An equal number of CD25 − CXCR6 − cells or CD25 − CXCR6 + CD4 + T cell isolated from colon LP of colitic mice was retransferred into Rag1 −/− mice. ( B ) Time course of changes in body weight after retransfer of the two subsets or transfer of CD45RB high naïve T cells. CXCR6 – transferred Rag1 −/− mice manifested progressive body weight loss to a similar extent to CD45RB high -transferred Rag1 −/− mice, whereas the cohort that received CXCR6 + cells did not show wasting. Data are expressed as the mean and s.e.m of two independent experiments. *, P < 0.05 ***, P < 0.001 versus CXCR6 + -transferred animals. ( C ) Histopathological analysis of distal colon tissue at 8 weeks post transfer. The transfer of CXCR6 − CD4 + T cells alone induced intestinal inflammation. Scale bars, 50 µm. ( D ) Number of CD4 + T cells in each group were calculated based on the flow cytometric analysis. ( E ) CXCR6 expression on CD4 + T cells in each group was analyzed by flow cytometry using CXCL16-hFc at 8-week post transfer. CXCR6 − CD4 + T cells express CXCR6 upon retransfer. ( F ) Intracellular cytokine staining was performed in LP CD4 + T cells in recipients of CXCR6 − CD4 + T cells at 8 weeks after transfer. The CXCR6 − subset produced IFN-γ and IL-17A coincident with the expression of CXCR6 upon retransfer. ( G ) LP CXCR6 − and CXCR6 + subsets were purified from CD45RB high -transferred Rag1 −/− mice at 8-week post transfer, labeled with CFSE and cultured with LP MHC class II + CD11c + cells at a 5∶1 ratio in the presence of 5 µg/ml anti-CD3ε Abs and 20 ng/ml IL-23 for 3 days. Proliferation was measured by CFSE dilution. Proliferation by CXCR6 − and CXCR6 + cells is depicted in the right columns. All data are representative from four independent experiments (mean and s.d.).

Journal: PLoS ONE

Article Title: Distinct Roles for CXCR6 + and CXCR6 − CD4 + T Cells in the Pathogenesis of Chronic Colitis

doi: 10.1371/journal.pone.0065488

Figure Lengend Snippet: ( A ) Schematic transfer protocol. An equal number of CD25 − CXCR6 − cells or CD25 − CXCR6 + CD4 + T cell isolated from colon LP of colitic mice was retransferred into Rag1 −/− mice. ( B ) Time course of changes in body weight after retransfer of the two subsets or transfer of CD45RB high naïve T cells. CXCR6 – transferred Rag1 −/− mice manifested progressive body weight loss to a similar extent to CD45RB high -transferred Rag1 −/− mice, whereas the cohort that received CXCR6 + cells did not show wasting. Data are expressed as the mean and s.e.m of two independent experiments. *, P < 0.05 ***, P < 0.001 versus CXCR6 + -transferred animals. ( C ) Histopathological analysis of distal colon tissue at 8 weeks post transfer. The transfer of CXCR6 − CD4 + T cells alone induced intestinal inflammation. Scale bars, 50 µm. ( D ) Number of CD4 + T cells in each group were calculated based on the flow cytometric analysis. ( E ) CXCR6 expression on CD4 + T cells in each group was analyzed by flow cytometry using CXCL16-hFc at 8-week post transfer. CXCR6 − CD4 + T cells express CXCR6 upon retransfer. ( F ) Intracellular cytokine staining was performed in LP CD4 + T cells in recipients of CXCR6 − CD4 + T cells at 8 weeks after transfer. The CXCR6 − subset produced IFN-γ and IL-17A coincident with the expression of CXCR6 upon retransfer. ( G ) LP CXCR6 − and CXCR6 + subsets were purified from CD45RB high -transferred Rag1 −/− mice at 8-week post transfer, labeled with CFSE and cultured with LP MHC class II + CD11c + cells at a 5∶1 ratio in the presence of 5 µg/ml anti-CD3ε Abs and 20 ng/ml IL-23 for 3 days. Proliferation was measured by CFSE dilution. Proliferation by CXCR6 − and CXCR6 + cells is depicted in the right columns. All data are representative from four independent experiments (mean and s.d.).

Techniques: Isolation, Expressing, Flow Cytometry, Staining, Produced, Purification, Labeling, Cell Culture

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1) Product Images from "Chemokine CXCL16 mediates acinar cell necrosis in cerulein induced acute pancreatitis in mice"

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