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Sino Biological human dcir clec4a protein fc tag
Human Dcir Clec4a Protein Fc Tag, supplied by Sino Biological, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+dcir/Human+CLEC4A+Protein/pmc10602528__ADVS___10___2303832___s002-91-9-16
Average 91 stars, based on 1 article reviews

human dcir clec4a protein fc tag - by Bioz Stars, 2026-09

91/100 stars

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Article Title: N‐glycan in cockroach allergen regulates human basophil function
Article Snippet: EIA/RIA 96‐well flat bottom plates (Costar) were coated in duplicate with 10 ug/mL of CRE, mannan‐BSA, or BSA for 18 h at 4°C, blocked with 1% BSA in TBST with 100 ug/mL of CaCl 2 for 1 h at room temperature. .. Purified recombinant human DCIR‐6xHis (Sino Biological, Beijing, P.R.China) dissolved in blocking buffer was incubated for 1 h at room temperature, washed, and incubated with horseradish peroxidase‐conjugated anti‐6xHis (Santa Cruz Biotechnology, Santa Cruz, CA, USA). .. The absorbance was recorded at 450 nm in an ELISA reader (BioRad, Hercules, CA, USA).

Article Title: Dendritic cell immunoreceptor drives atopic dermatitis by modulating oxidized CaMKII-involved mast cell activation
Article Snippet: Enzyme immunoassay/radioimmunoassay (EIA/RIA) 96-well flat-bottom plates (Costar) were coated in duplicate with 10 μg/mL of CRE, mannan-BSA, or BSA in PBS overnight at 4 o C. The plate was blocked with 1% BSA in TBST for 1 hour at RT. .. Various concentrations of purified recombinant human DCIR-6xHis (Sino Biological) dissolved in blocking buffer with 100 μg/mL of CaCl 2 were incubated for 1 hour at RT. .. The plate was washed and incubated with anti–6xHis horseradish peroxidase–conjugated IgG (MAB050H, R&D Systems; ).

Recombinant:

Blocking Assay:

Incubation:

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( A ) Relative DCIR mRNA expression in blood immune cells (BLUEPRINT data set). ( B ) Flow cytometry analysis of DCIR expressed in the neutrophils, monocytes, and T and B cells isolated from human PBMCs with or without 100 ng/mL LPS stimulation for 1 hour ( n = 3 for isotype staining control, n = 5 for PBS or LPS-treated group). Means ± SEM are shown, and statistical analysis is determined by 1-way ANOVA test with Dunnett’s correction compared with the isotype staining control. *** P < 0.001. ( C ) t-SNE plot of single-cell RNA-Seq analysis for skin biopsy collected from hidradenitis suppurativa (HS) patients (GSE155850). ( D ) DCIR-expressing cells overlaying on t-SNE plot of the single-cell RNA-Seq analysis for the normal adjacent tissue or skin lesion from patients with HS. DCIR mRNA level in the different cell clusters were quantitated by pseudo-bulk differential expression analysis based on scRNA-Seq results as described in C . ( E ) Representative immunohistochemical staining of DCIR + cells in normal or disease skin tissues of HS. ( F ) Immunohistochemical staining of DCIR + cells in skin lesion of HS and SLE, and mucosal tissue of CD. Scale bars: 100 μm.

Journal: JCI Insight

Article Title: Agonistic anti-DCIR antibody inhibits ITAM-mediated inflammatory signaling and promotes immune resolution

doi: 10.1172/jci.insight.176064

Figure Lengend Snippet: ( A ) Relative DCIR mRNA expression in blood immune cells (BLUEPRINT data set). ( B ) Flow cytometry analysis of DCIR expressed in the neutrophils, monocytes, and T and B cells isolated from human PBMCs with or without 100 ng/mL LPS stimulation for 1 hour ( n = 3 for isotype staining control, n = 5 for PBS or LPS-treated group). Means ± SEM are shown, and statistical analysis is determined by 1-way ANOVA test with Dunnett’s correction compared with the isotype staining control. *** P < 0.001. ( C ) t-SNE plot of single-cell RNA-Seq analysis for skin biopsy collected from hidradenitis suppurativa (HS) patients (GSE155850). ( D ) DCIR-expressing cells overlaying on t-SNE plot of the single-cell RNA-Seq analysis for the normal adjacent tissue or skin lesion from patients with HS. DCIR mRNA level in the different cell clusters were quantitated by pseudo-bulk differential expression analysis based on scRNA-Seq results as described in C . ( E ) Representative immunohistochemical staining of DCIR + cells in normal or disease skin tissues of HS. ( F ) Immunohistochemical staining of DCIR + cells in skin lesion of HS and SLE, and mucosal tissue of CD. Scale bars: 100 μm.

Article Snippet: Antibodies used for FACS analysis include PE-Cy7 anti–human CD11b (101216, BioLegend), APC anti–human CD66b (392912, BioLegend), APC-Cy7 anti–human HLA-DR (307618, BioLegend), APC anti–human CD16 (302012, BioLegend), FITC anti–human CD14 (325603, BioLegend), APC-Cy7 anti–human CD3 (300318, BioLegend), BV510 anti–human CD19 (302242, BioLegend), AF488 anti–mouse Ly-6G (127626, BioLegend), PE anti–human DCIR (FAB1748P, R&D system), PE rat anti–mouse DCIR1 (Clec4a2) (566810, BD Bioscience), APC anti–human IgG (H+L) (109-136-088, Jackson ImmunoResearch), and PE anti–human IgG Fcγ fragment specific ((09-115-098, Jackson ImmunoResearch).

Techniques: Expressing, Flow Cytometry, Isolation, Staining, Control, RNA Sequencing, Quantitative Proteomics, Immunohistochemical staining

( A ) Graphic of the agonistic effect induced by anti-DCIR mAbs. ( B and C ) WT and huDCIR transfected HEK293 cells were treated with anti-DCIR mAbs (10 μg/mL) for 30 minutes, followed by immunoprecipitation assay (IP) with anti-phosphorylated tyrosine ( B ) or anti-SHP2 ( C ) antibodies. DCIR levels were analyzed by WB and quantitated by densitometry. Representative data from 2 independent studies are shown. ( D ) Illustration of the huDCIR agonistic effect reporter cell generation. HEK293 cell was cotransfected with a huDCIR vector containing an ITAM motif cloned from Dectin-1 and a luciferase reporter vector with NF-кB response element. ( E ) Reporter cells as described in D were treated with 10 μg/mL anti-DCIR mAbs or isotype control for 30 minutes, followed by luciferase assay analysis. Agonistic effects induced by the antibodies were quantitated by the luminescent signal. ( F ) Reporter cells as described in D were treated with a serial dilution of agonistic or nonagonistic anti-DCIR antibodies or isotype control for 30 minutes, followed by luciferase assay analysis. Dose-dependent induction of agonistic signaling was quantitated by the luminescent signal. ( G and H ) DCIR ligands, mannose and asialo-biantennary N-glycan (NA2-glycan), were conjugated with BSA and immobilized on culture plates. Dose-dependent agonistic effects of mannose-BSA and NA2 glycan-BSA were determined by the reporter system as described in D . ( I ) In total, 50 μg/mL of mannose-BSA and NA2 glycan-BSA were coated on the cell culture plate and cultured with HEK293 cells contain the huDCIR-agonist reporter for 6 hours. Agonistic effects induced by anti-DCIR antibody (9D9) were determined by luciferase assay after overnight culture. ( E – I ) Representative data from 2 independent studies are shown. Means ± SEM from triplicates are shown.

Journal: JCI Insight

Article Title: Agonistic anti-DCIR antibody inhibits ITAM-mediated inflammatory signaling and promotes immune resolution

doi: 10.1172/jci.insight.176064

Figure Lengend Snippet: ( A ) Graphic of the agonistic effect induced by anti-DCIR mAbs. ( B and C ) WT and huDCIR transfected HEK293 cells were treated with anti-DCIR mAbs (10 μg/mL) for 30 minutes, followed by immunoprecipitation assay (IP) with anti-phosphorylated tyrosine ( B ) or anti-SHP2 ( C ) antibodies. DCIR levels were analyzed by WB and quantitated by densitometry. Representative data from 2 independent studies are shown. ( D ) Illustration of the huDCIR agonistic effect reporter cell generation. HEK293 cell was cotransfected with a huDCIR vector containing an ITAM motif cloned from Dectin-1 and a luciferase reporter vector with NF-кB response element. ( E ) Reporter cells as described in D were treated with 10 μg/mL anti-DCIR mAbs or isotype control for 30 minutes, followed by luciferase assay analysis. Agonistic effects induced by the antibodies were quantitated by the luminescent signal. ( F ) Reporter cells as described in D were treated with a serial dilution of agonistic or nonagonistic anti-DCIR antibodies or isotype control for 30 minutes, followed by luciferase assay analysis. Dose-dependent induction of agonistic signaling was quantitated by the luminescent signal. ( G and H ) DCIR ligands, mannose and asialo-biantennary N-glycan (NA2-glycan), were conjugated with BSA and immobilized on culture plates. Dose-dependent agonistic effects of mannose-BSA and NA2 glycan-BSA were determined by the reporter system as described in D . ( I ) In total, 50 μg/mL of mannose-BSA and NA2 glycan-BSA were coated on the cell culture plate and cultured with HEK293 cells contain the huDCIR-agonist reporter for 6 hours. Agonistic effects induced by anti-DCIR antibody (9D9) were determined by luciferase assay after overnight culture. ( E – I ) Representative data from 2 independent studies are shown. Means ± SEM from triplicates are shown.

Techniques: Transfection, Immunoprecipitation, Plasmid Preparation, Clone Assay, Luciferase, Control, Serial Dilution, Glycoproteomics, Cell Culture

( A ) Human monocytes were treated with 5 μg/mL antibodies for 30 minutes. Antibody binding was quantitated by the 10 μg/mL PE anti-human IgG secondary antibody. Data are normalized to the isotype group. Representative data from 2 independent studies are shown. ( B ) Scheme of the immunosuppressive effect induced by the agonistic anti-DCIR mAb. ( C ) Human monocytes were treated with 5 μg/mL anti-DCIR mAbs or isotype for 30 minutes, followed by immunoprecipitation (IP) using anti-SHP2 antibody. SHP2-DCIR interaction was evaluated by the DCIR level analyzed by WB. SHP2 from IP lysate and GAPDH from whole cell lysate were probed as loading controls. ( D and E ) Human monocytes were pretreated with 5 μg/mL antibodies for 30 minutes, followed by 50 μg/mL anti-human IC: HSA stimulation for 30 minutes. SYK’s interactions with SHP2 and FcRγ chain were evaluated by immunoprecipitation using anti-SHP2 ( D ) and anti-FcRγ ( E ) antibodies. SHP2 and FcRγ chain from IP lysate and Actin from whole cell lysate were probed as loading controls. ( A and C – E ) Representative data from 2 studies are shown. ( F and G ) Human monocytes ( n = 3) were pretreated with 10 μg/mL antibodies for 30 minutes, followed by 25 μg/mL ZymD stimulation overnight. Induction of TNF-α and IL-6 in supernatant were measured by ELISA and normalized to the isotype group. ( H ) Human neutrophils were pretreated with 10 μg/mL antibodies for 2 hours, and OCR were detected in real time after GM-CSF/PMA stimulation. AUC of the OCR was shown. Representative data from 3 independent studies are shown. ( F – H ) Means ± SEM are shown, and statistical significance is determined by 1-way ANOVA test with Dunnett’s correction compared with the isotype condition. * P < 0.05, ** P < 0.01.

Journal: JCI Insight

Article Title: Agonistic anti-DCIR antibody inhibits ITAM-mediated inflammatory signaling and promotes immune resolution

doi: 10.1172/jci.insight.176064

Figure Lengend Snippet: ( A ) Human monocytes were treated with 5 μg/mL antibodies for 30 minutes. Antibody binding was quantitated by the 10 μg/mL PE anti-human IgG secondary antibody. Data are normalized to the isotype group. Representative data from 2 independent studies are shown. ( B ) Scheme of the immunosuppressive effect induced by the agonistic anti-DCIR mAb. ( C ) Human monocytes were treated with 5 μg/mL anti-DCIR mAbs or isotype for 30 minutes, followed by immunoprecipitation (IP) using anti-SHP2 antibody. SHP2-DCIR interaction was evaluated by the DCIR level analyzed by WB. SHP2 from IP lysate and GAPDH from whole cell lysate were probed as loading controls. ( D and E ) Human monocytes were pretreated with 5 μg/mL antibodies for 30 minutes, followed by 50 μg/mL anti-human IC: HSA stimulation for 30 minutes. SYK’s interactions with SHP2 and FcRγ chain were evaluated by immunoprecipitation using anti-SHP2 ( D ) and anti-FcRγ ( E ) antibodies. SHP2 and FcRγ chain from IP lysate and Actin from whole cell lysate were probed as loading controls. ( A and C – E ) Representative data from 2 studies are shown. ( F and G ) Human monocytes ( n = 3) were pretreated with 10 μg/mL antibodies for 30 minutes, followed by 25 μg/mL ZymD stimulation overnight. Induction of TNF-α and IL-6 in supernatant were measured by ELISA and normalized to the isotype group. ( H ) Human neutrophils were pretreated with 10 μg/mL antibodies for 2 hours, and OCR were detected in real time after GM-CSF/PMA stimulation. AUC of the OCR was shown. Representative data from 3 independent studies are shown. ( F – H ) Means ± SEM are shown, and statistical significance is determined by 1-way ANOVA test with Dunnett’s correction compared with the isotype condition. * P < 0.05, ** P < 0.01.

Techniques: Binding Assay, Immunoprecipitation, Enzyme-linked Immunosorbent Assay

( A ) Illustration of the huDCIR-KI mice generation. ( B ) Flow cytometry of huDCIR expressed in pooled BM spleen, or blood CD11b + cells from WT or homogenous huDCIR-KI mice (HO). ( C – E ) Flow cytometry of huDCIR and tdTomato expressed in the monocytes (CD11b + Ly6G – ), neutrophils (CD1b + Ly6G + ), and DCIR + and DCIR – cells from the BM of WT or homogenous huDCIR-KI mice. ( F ) Design of the peritonitis model induced by i.p. injection of 0.5 mL 2 mg/mL ZymD. ( G ) Flow cytometry quantitation of huDCIR-expressing (tdTomato + ) cells in the CD45 + leukocytes isolated from the peritoneal lavage of WT and homogenous huDCIR-KI mice in the peritonitis model as described in F . Means ± SEM are shown, and statistical analysis is determined by 1-way ANOVA test with Dunnett’s correction compared with the PBS treated huDCIR-KI group. * P < 0.05, *** P < 0.001. ( H ) Design of the DSS-colitis model. Mice were fed 3% DSS in drinking water for 7 days. For the vessel staining, mice were i.v. administrated with 100 μL of 1 mg/mL 10 kDa AF680 dextran 2 days before feeding DSS water. For the DCIR + cells detection, AF488 anti-DCIR mAb were i.v. injected into the mice 3 days before and 6 days after DSS feeding. CLE analyses were performed on day 0 (naive) and day 7 (colitis) during the DSS-feeding phase. ( I ) Representative CLE of naïve mice and mice with colitis as described in F . DCIR + cells in the colonic crypts were stained with AF488 anti-DCIR mAb (green), and blood vessels running along the crypt wall were stained with AF680 dextran (red). Scale bars: 20 μm.

Journal: JCI Insight

Article Title: Agonistic anti-DCIR antibody inhibits ITAM-mediated inflammatory signaling and promotes immune resolution

doi: 10.1172/jci.insight.176064

Figure Lengend Snippet: ( A ) Illustration of the huDCIR-KI mice generation. ( B ) Flow cytometry of huDCIR expressed in pooled BM spleen, or blood CD11b + cells from WT or homogenous huDCIR-KI mice (HO). ( C – E ) Flow cytometry of huDCIR and tdTomato expressed in the monocytes (CD11b + Ly6G – ), neutrophils (CD1b + Ly6G + ), and DCIR + and DCIR – cells from the BM of WT or homogenous huDCIR-KI mice. ( F ) Design of the peritonitis model induced by i.p. injection of 0.5 mL 2 mg/mL ZymD. ( G ) Flow cytometry quantitation of huDCIR-expressing (tdTomato + ) cells in the CD45 + leukocytes isolated from the peritoneal lavage of WT and homogenous huDCIR-KI mice in the peritonitis model as described in F . Means ± SEM are shown, and statistical analysis is determined by 1-way ANOVA test with Dunnett’s correction compared with the PBS treated huDCIR-KI group. * P < 0.05, *** P < 0.001. ( H ) Design of the DSS-colitis model. Mice were fed 3% DSS in drinking water for 7 days. For the vessel staining, mice were i.v. administrated with 100 μL of 1 mg/mL 10 kDa AF680 dextran 2 days before feeding DSS water. For the DCIR + cells detection, AF488 anti-DCIR mAb were i.v. injected into the mice 3 days before and 6 days after DSS feeding. CLE analyses were performed on day 0 (naive) and day 7 (colitis) during the DSS-feeding phase. ( I ) Representative CLE of naïve mice and mice with colitis as described in F . DCIR + cells in the colonic crypts were stained with AF488 anti-DCIR mAb (green), and blood vessels running along the crypt wall were stained with AF680 dextran (red). Scale bars: 20 μm.

Techniques: Flow Cytometry, Injection, Quantitation Assay, Expressing, Isolation, Staining

( A ) Study design of the prophylactic anti-DCIR mAbs treatment in the ZymD-induced peritonitis model. Anti-DCIR mAbs and Fc-matched isotype control were i.p. injected into the mice 1 day before the i.p. administration of 0.5 mL 2 mg/mL ZymD to induce peritonitis. ( B – G ) Relative leukocyte and neutrophil infiltration ( B and C ) and cytokine production in the peritoneal lavage ( D – G ) collected from the mice received i.p. administration of 10 mpk anti-DCIR mAbs clone 9D9 ( n = 6 huDCIR-KI mice), 3A4 ( n = 4 WT or n = 22 huDCIR-KI mice), 3F7 ( n = 6 huDCIR-KI mice), or isotype ( n = 5 WT or 14 huDCIR-KI mice) in the peritonitis model as described in A . ( H – M ) Relative leukocytes and neutrophils infiltration ( H and I ) and cytokine production in the peritoneal lavage ( J – M ) isolated from the mice received 10 mpk i.p. administration of agonistic anti-DCIR mAb clone 3A4 with WT ( n = 22) or LALA (L234A and L235A) mutant huIgG1 Fc ( n = 6) or isotype ( n = 31) in the peritonitis model as described in A . Data are normalized to the isotype group. Each datum represents an individual mouse treated with indicated condition. Means ± SEM are shown, and statistical significance is determined by 1-way ANOVA test with Dunnett’s correction for multiple comparison to the isotype treated condition. * P < 0.05, ** P < 0.01, *** P < 0.001.

Journal: JCI Insight

Article Title: Agonistic anti-DCIR antibody inhibits ITAM-mediated inflammatory signaling and promotes immune resolution

doi: 10.1172/jci.insight.176064

Figure Lengend Snippet: ( A ) Study design of the prophylactic anti-DCIR mAbs treatment in the ZymD-induced peritonitis model. Anti-DCIR mAbs and Fc-matched isotype control were i.p. injected into the mice 1 day before the i.p. administration of 0.5 mL 2 mg/mL ZymD to induce peritonitis. ( B – G ) Relative leukocyte and neutrophil infiltration ( B and C ) and cytokine production in the peritoneal lavage ( D – G ) collected from the mice received i.p. administration of 10 mpk anti-DCIR mAbs clone 9D9 ( n = 6 huDCIR-KI mice), 3A4 ( n = 4 WT or n = 22 huDCIR-KI mice), 3F7 ( n = 6 huDCIR-KI mice), or isotype ( n = 5 WT or 14 huDCIR-KI mice) in the peritonitis model as described in A . ( H – M ) Relative leukocytes and neutrophils infiltration ( H and I ) and cytokine production in the peritoneal lavage ( J – M ) isolated from the mice received 10 mpk i.p. administration of agonistic anti-DCIR mAb clone 3A4 with WT ( n = 22) or LALA (L234A and L235A) mutant huIgG1 Fc ( n = 6) or isotype ( n = 31) in the peritonitis model as described in A . Data are normalized to the isotype group. Each datum represents an individual mouse treated with indicated condition. Means ± SEM are shown, and statistical significance is determined by 1-way ANOVA test with Dunnett’s correction for multiple comparison to the isotype treated condition. * P < 0.05, ** P < 0.01, *** P < 0.001.

Techniques: Control, Injection, Isolation, Mutagenesis, Comparison

( A ) LPS primed human neutrophils were labeled CellTracker Green. Neutrophils were incubated with 5 μg/mL anti-DCIR mAbs (3A4, 9D9, 5E11, 3F7) or isotype for 30 minutes on ice. Neutrophils and monocyte-derived macrophages were cocultured (ratio 4:1). ( B ) ADCP were quantitated by flow cytometry detecting CellTracker Green + CD11b + CD66b – HLA-DR + macrophage after 2 hours coculture with 3A4 ( n = 12), 9D9 ( n = 6), 5E11 ( n = 6), 3F7( n = 12), or isotype ( n = 11). Data are normalized to 3A4 group. ( C ) LPS primed neutrophils were incubated with 3A4, 9D9, 5E11, 3F7, or isotype for 30 minutes on ice. Neutrophils and Jurkat cells containing an ADCC reporter were cocultured (ratio 4:1). ( D ) ADCC were quantitated by luminescence overnight. Representative data from 2 studies are shown. ( E ) Confocal flow cytometry of human monocytes treated with 10 μg/mL A647-labeled antibodies (red) for 0, 15, and 30 minutes at 37°C. Antibody internalization was determined by colocalization (yellow) of A647-labeled antibodies in lysosome, marked by A488 anti-LAMP1 antibody (green). ( F and G ) HuDCIR-KI mice received i.p. administration of 10 mpk 5E11 with WT ( n = 25) or LALA mutant ( n = 7) huIgG1 Fc or isotype ( n = 25) 1 day before the i.p. injection of 0.5 mL 2 mg/mL ZymD. Relative leukocytes and neutrophils induction in peritoneal lavage were quantitated 6 hours after the ZymD injection. Data are normalized to isotype group. ( H – K ) Relative leukocytes and neutrophils infiltration ( H and I ) and cytokine in peritoneal fluid ( J and K ) collected 6 hours after ZymD injection, from mice pretreated with 5E11 with mouse IgG2b (5E11-mIgG2b) ( n = 5), Fc-matched isotype (iso-mIgG2b) ( n = 5), or anti–Gr-1 mAb (RB6-8C5) ( n = 5) 1 day before the peritonitis. Data are normalized to isotype group. Each dot represents 1 biological replicate. Means ± SEM are shown, and statistical significance is determined by 1-way ANOVA with Dunnett’s correction compared with the isotype condition. * P < 0.05, ** P < 0.01, *** P < 0.001.

Journal: JCI Insight

Article Title: Agonistic anti-DCIR antibody inhibits ITAM-mediated inflammatory signaling and promotes immune resolution

doi: 10.1172/jci.insight.176064

Figure Lengend Snippet: ( A ) LPS primed human neutrophils were labeled CellTracker Green. Neutrophils were incubated with 5 μg/mL anti-DCIR mAbs (3A4, 9D9, 5E11, 3F7) or isotype for 30 minutes on ice. Neutrophils and monocyte-derived macrophages were cocultured (ratio 4:1). ( B ) ADCP were quantitated by flow cytometry detecting CellTracker Green + CD11b + CD66b – HLA-DR + macrophage after 2 hours coculture with 3A4 ( n = 12), 9D9 ( n = 6), 5E11 ( n = 6), 3F7( n = 12), or isotype ( n = 11). Data are normalized to 3A4 group. ( C ) LPS primed neutrophils were incubated with 3A4, 9D9, 5E11, 3F7, or isotype for 30 minutes on ice. Neutrophils and Jurkat cells containing an ADCC reporter were cocultured (ratio 4:1). ( D ) ADCC were quantitated by luminescence overnight. Representative data from 2 studies are shown. ( E ) Confocal flow cytometry of human monocytes treated with 10 μg/mL A647-labeled antibodies (red) for 0, 15, and 30 minutes at 37°C. Antibody internalization was determined by colocalization (yellow) of A647-labeled antibodies in lysosome, marked by A488 anti-LAMP1 antibody (green). ( F and G ) HuDCIR-KI mice received i.p. administration of 10 mpk 5E11 with WT ( n = 25) or LALA mutant ( n = 7) huIgG1 Fc or isotype ( n = 25) 1 day before the i.p. injection of 0.5 mL 2 mg/mL ZymD. Relative leukocytes and neutrophils induction in peritoneal lavage were quantitated 6 hours after the ZymD injection. Data are normalized to isotype group. ( H – K ) Relative leukocytes and neutrophils infiltration ( H and I ) and cytokine in peritoneal fluid ( J and K ) collected 6 hours after ZymD injection, from mice pretreated with 5E11 with mouse IgG2b (5E11-mIgG2b) ( n = 5), Fc-matched isotype (iso-mIgG2b) ( n = 5), or anti–Gr-1 mAb (RB6-8C5) ( n = 5) 1 day before the peritonitis. Data are normalized to isotype group. Each dot represents 1 biological replicate. Means ± SEM are shown, and statistical significance is determined by 1-way ANOVA with Dunnett’s correction compared with the isotype condition. * P < 0.05, ** P < 0.01, *** P < 0.001.

Techniques: Labeling, Incubation, Derivative Assay, Flow Cytometry, Mutagenesis, Injection

( A ) Study design of murine DSS-induced colitis model with prophylactic anti-DCIR mAbs treatment. huDCIR-KI mice were i.p. injected with 10 mpk anti-DCIR mAbs (9D9, 3F7) or isotype control ( n = 5/antibody-treated group) on day 0 and 3 during the 7 days long 3%DSS water feeding period. ( B ) Body weight change of the mice treated with indicated antibodies during the DSS-colitis phase. Weight is presented relative to the initial body weight before DSS-water feeding. ( C ) Representative confocal laser endoscopy (CLE) image of the colonic crypts (green, labeled by Acriflavine) with infiltrated inflammatory neutrophils (red, labeled by NE680) from mice received 3%DSS for 7 days with different colitis severity. ( D and E ) Representative CLE image of colonic crypts with associated neutrophil activation score indicated by the NE680 staining ( D ), and representative H&E-stained colons ( E ) with associated histology score of the mice received anti-DCIR mAbs and isotype control treatment as illustrated in A . Scale bars: 20 μm for D and 100 μm for E . M, mucosal gland; SM, submucosa; TME, tunica muscularis externa; thin arrows, erosion; thick arrows, inflammatory cells; **, gland loss. ( F ) MIP-2 cytokine level in mice serum collected on day7 after the DSS-colitis. Data are normalized to isotype group. Each data point represents the individual mouse treated with indicated condition. Means ± SEM are shown, and statistical significance is determined by 1-way ANOVA test with Dunnett’s correction for multiple comparison to the isotype treated condition. * P < 0.05, *** P < 0.001.

Journal: JCI Insight

Article Title: Agonistic anti-DCIR antibody inhibits ITAM-mediated inflammatory signaling and promotes immune resolution

doi: 10.1172/jci.insight.176064

Figure Lengend Snippet: ( A ) Study design of murine DSS-induced colitis model with prophylactic anti-DCIR mAbs treatment. huDCIR-KI mice were i.p. injected with 10 mpk anti-DCIR mAbs (9D9, 3F7) or isotype control ( n = 5/antibody-treated group) on day 0 and 3 during the 7 days long 3%DSS water feeding period. ( B ) Body weight change of the mice treated with indicated antibodies during the DSS-colitis phase. Weight is presented relative to the initial body weight before DSS-water feeding. ( C ) Representative confocal laser endoscopy (CLE) image of the colonic crypts (green, labeled by Acriflavine) with infiltrated inflammatory neutrophils (red, labeled by NE680) from mice received 3%DSS for 7 days with different colitis severity. ( D and E ) Representative CLE image of colonic crypts with associated neutrophil activation score indicated by the NE680 staining ( D ), and representative H&E-stained colons ( E ) with associated histology score of the mice received anti-DCIR mAbs and isotype control treatment as illustrated in A . Scale bars: 20 μm for D and 100 μm for E . M, mucosal gland; SM, submucosa; TME, tunica muscularis externa; thin arrows, erosion; thick arrows, inflammatory cells; **, gland loss. ( F ) MIP-2 cytokine level in mice serum collected on day7 after the DSS-colitis. Data are normalized to isotype group. Each data point represents the individual mouse treated with indicated condition. Means ± SEM are shown, and statistical significance is determined by 1-way ANOVA test with Dunnett’s correction for multiple comparison to the isotype treated condition. * P < 0.05, *** P < 0.001.

Techniques: Injection, Control, Labeling, Activation Assay, Staining, Comparison

Figure 1. Represented the ratios (a), median fluorescence intensity (MFI) (b) and adjusted expression (c) of C5AR1, CLEC4A and NLRP3 to CD3+ lymphocytes between healthy controls (n = 44) and early-stage NSCLC patients (n = 63). The ROC curve of C5AR1, CLEC4A and NLRP3 ratio and MFI between healthy controls and early-stage NSCLC patient (c,d). The CD3+NLRP3+ MFI provided the most distinguishable between early-stage NSCLC and healthy volunteer at 71.5% sensitivity and 70% specificity.

Journal: Scientific reports

Article Title: Differential expression of immune-regulatory proteins C5AR1, CLEC4A and NLRP3 on peripheral blood mononuclear cells in early-stage non-small cell lung cancer patients.

doi: 10.1038/s41598-022-21891-0

Figure Lengend Snippet: Figure 1. Represented the ratios (a), median fluorescence intensity (MFI) (b) and adjusted expression (c) of C5AR1, CLEC4A and NLRP3 to CD3+ lymphocytes between healthy controls (n = 44) and early-stage NSCLC patients (n = 63). The ROC curve of C5AR1, CLEC4A and NLRP3 ratio and MFI between healthy controls and early-stage NSCLC patient (c,d). The CD3+NLRP3+ MFI provided the most distinguishable between early-stage NSCLC and healthy volunteer at 71.5% sensitivity and 70% specificity.

Article Snippet: For the extracellular staining, the pellets were resuspended with 3% FBS in 1X PBS and stained with human CD3 (1 μg APC anti-human CD3 antibody, Biolegend), C5aR (1 μg PE/Cyanine7 anti-human CD88 antibody, Biolegend), CLEC4A (1 μg Alexa Fluor® 488 anti-human DCIR/CLEC4A antibody, R&D systems), and cell viability (1 μg 7-AAD Viability Staining Solution, Biolegend) at 4 °C for 2 h in darkness.

Techniques: Fluorescence, Expressing

Figure 2. Represented the ratios (a), median fluorescence intensity (b) and adjusted expression (c) of C5AR1, CLEC4A and NLRP3 proteins on CD3+ lymphocytes between non-malignant pulmonary diseases (n = 10) and early-stage NSCLC patients (n = 63). Median fluorescence intensity of CD3+NLRP3+ in early-stage NSCLC patients was 1585 [range 478–5224] which was higher than non-malignant pulmonary diseases, 899 [range 354– 1888, p = 0.01]. The limited number of patients with non-malignant pulmonary disease in our study impacted the ability to show if PBMCs protein expression as a biomarker could discriminate between these conditions.

Journal: Scientific reports

Article Title: Differential expression of immune-regulatory proteins C5AR1, CLEC4A and NLRP3 on peripheral blood mononuclear cells in early-stage non-small cell lung cancer patients.

doi: 10.1038/s41598-022-21891-0

Figure Lengend Snippet: Figure 2. Represented the ratios (a), median fluorescence intensity (b) and adjusted expression (c) of C5AR1, CLEC4A and NLRP3 proteins on CD3+ lymphocytes between non-malignant pulmonary diseases (n = 10) and early-stage NSCLC patients (n = 63). Median fluorescence intensity of CD3+NLRP3+ in early-stage NSCLC patients was 1585 [range 478–5224] which was higher than non-malignant pulmonary diseases, 899 [range 354– 1888, p = 0.01]. The limited number of patients with non-malignant pulmonary disease in our study impacted the ability to show if PBMCs protein expression as a biomarker could discriminate between these conditions.

Techniques: Fluorescence, Expressing, Biomarker Discovery

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human dcir clec4a protein fc tag (Sino Biological)

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