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( A ) Expression of CD27 and IgD on CD19 + B cells. Right: Percentage of IgD + CD27 − naïve B cells and IgD − CD27 − DN B cells. ( B ) Expression of CD27 and CD38 on CD19 + B cells. Right: Percentages of CD27 hi CD38 hi ASCs and CD27 + CD38 − memory B cells. ( C ) Expression of CD138 on CD27 hi CD38 hi ASCs. Right: Percentage of CD138 + ASCs and CD138 − ASCs. ( D ) Expression of CD11c and CD21 on CD19 + B cells. Right: Percentage of CD11c + CD21 − CD19 + B cells. [(A) to (D)] HC ( n = 63), irAE ( n = 33), RAC ( n = 46), and ICI ( n = 20). ( E to G ) GSEA was performed on the B cells between irAE and ICI. (E) Significantly enriched pathways in B cells from irAE and ICI. GSEA plots of IFN-α and IFN-γ response (F), and oxidative phosphorylation (G). ( H ) The volcano plots of the citrullinated or noncitrullinated relative <t>IgG</t> or IgM isotype autoantigen levels comparing RA versus HC, irAE versus ICI, irAE versus HC, or irAE versus RA. The autoantigens were labeled when P < 0.01. TNF-α reactivities resulted from the administration of anti–TNF-α therapy for the treatment of RA. ( I ) Immunoglobulin isotype levels in the plasma were measured by multiplex assay. HC ( n = 22), irAE ( n = 34), RAC ( n = 46), and ICI ( n = 26). ( J ) CXCL13 levels in the plasma were measured by enzyme-linked immunosorbent assay (ELISA). HC ( n = 20), irAE ( n = 34) RAC ( n = 47), and ICI ( n = 23). ( K ) B-cell activating factor (BAFF) levels in the plasma were measured by multiplex assay. HC ( n = 21), irAE ( n = 34), RAC ( n = 47), and ICI ( n = 18). Data in graphs represent mean ± SEM. Significance was tested by one-way ANOVA [(A) to (D) and (I) to (K)] and logistic regression (H). [(A) to (D) and (F) to (K)] ICI, ICI control.

Isotype Control Igg4, supplied by Bio X Cell, used in various techniques. Bioz Stars score: 94/100, based on 15 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Inflammatory arthritis irAE may represent a unique autoimmune disease primarily driven by T cells but likely not autoantibodies"

Article Title: Inflammatory arthritis irAE may represent a unique autoimmune disease primarily driven by T cells but likely not autoantibodies

Journal: Science Advances

doi: 10.1126/sciadv.aea4262

Figure Legend Snippet: ( A ) Expression of CD27 and IgD on CD19 + B cells. Right: Percentage of IgD + CD27 − naïve B cells and IgD − CD27 − DN B cells. ( B ) Expression of CD27 and CD38 on CD19 + B cells. Right: Percentages of CD27 hi CD38 hi ASCs and CD27 + CD38 − memory B cells. ( C ) Expression of CD138 on CD27 hi CD38 hi ASCs. Right: Percentage of CD138 + ASCs and CD138 − ASCs. ( D ) Expression of CD11c and CD21 on CD19 + B cells. Right: Percentage of CD11c + CD21 − CD19 + B cells. [(A) to (D)] HC ( n = 63), irAE ( n = 33), RAC ( n = 46), and ICI ( n = 20). ( E to G ) GSEA was performed on the B cells between irAE and ICI. (E) Significantly enriched pathways in B cells from irAE and ICI. GSEA plots of IFN-α and IFN-γ response (F), and oxidative phosphorylation (G). ( H ) The volcano plots of the citrullinated or noncitrullinated relative IgG or IgM isotype autoantigen levels comparing RA versus HC, irAE versus ICI, irAE versus HC, or irAE versus RA. The autoantigens were labeled when P < 0.01. TNF-α reactivities resulted from the administration of anti–TNF-α therapy for the treatment of RA. ( I ) Immunoglobulin isotype levels in the plasma were measured by multiplex assay. HC ( n = 22), irAE ( n = 34), RAC ( n = 46), and ICI ( n = 26). ( J ) CXCL13 levels in the plasma were measured by enzyme-linked immunosorbent assay (ELISA). HC ( n = 20), irAE ( n = 34) RAC ( n = 47), and ICI ( n = 23). ( K ) B-cell activating factor (BAFF) levels in the plasma were measured by multiplex assay. HC ( n = 21), irAE ( n = 34), RAC ( n = 47), and ICI ( n = 18). Data in graphs represent mean ± SEM. Significance was tested by one-way ANOVA [(A) to (D) and (I) to (K)] and logistic regression (H). [(A) to (D) and (F) to (K)] ICI, ICI control.

Techniques Used: Expressing, Phospho-proteomics, Immunopeptidomics, Labeling, Clinical Proteomics, Multiplex Assay, Enzyme-linked Immunosorbent Assay, Control

( A to C ) Human naïve B cells were isolated from PBMCs and cultured under indicated conditions for 7 days; pembrolizumab or isotype control IgG4 (IgG4 Iso) was added on day 2; n = 8. (A) Expression of CD38 and CD27 on B cells. Right: Percentages of CD27 + CD38 − and CD27 + CD38 + B cells. (B) Expression of CD138 on CD27 + CD38 + B cells. Right: Percentage of CD138 + CD27 + CD38 + B cells. (C) Different immunoglobulin isotypes were measured in the culture supernatant of (A) and (B) by multiplex assay. ( D to F ) B cells from Humanized PD-1 (HuPD-1) mice were isolated and cultured with LPS, IL-4, BAFF, or ODN 2006, anti-IgM, IL-21, IL-4 or R848, anti-IgM, anti-CD40, IL-21, and IFN-γ for 3 days; pembrolizumab or isotype control was added on day 1. (D) Expression of IgG2c on activated B cells. FSC-H, Forward scatter height. Right: Percentage of IgG2c + B cells; n = 5. (E) Expression of IgG1 on activated B cells. Right: Percentage of IgG1 + B cells; n = 5. (F) Different immunoglobulin isotypes in the supernatant were measured by multiplex assay; n = 5. Data in graphs represent mean ± SEM. Significance was tested by two-way ANOVA.

Figure Legend Snippet: ( A to C ) Human naïve B cells were isolated from PBMCs and cultured under indicated conditions for 7 days; pembrolizumab or isotype control IgG4 (IgG4 Iso) was added on day 2; n = 8. (A) Expression of CD38 and CD27 on B cells. Right: Percentages of CD27 + CD38 − and CD27 + CD38 + B cells. (B) Expression of CD138 on CD27 + CD38 + B cells. Right: Percentage of CD138 + CD27 + CD38 + B cells. (C) Different immunoglobulin isotypes were measured in the culture supernatant of (A) and (B) by multiplex assay. ( D to F ) B cells from Humanized PD-1 (HuPD-1) mice were isolated and cultured with LPS, IL-4, BAFF, or ODN 2006, anti-IgM, IL-21, IL-4 or R848, anti-IgM, anti-CD40, IL-21, and IFN-γ for 3 days; pembrolizumab or isotype control was added on day 1. (D) Expression of IgG2c on activated B cells. FSC-H, Forward scatter height. Right: Percentage of IgG2c + B cells; n = 5. (E) Expression of IgG1 on activated B cells. Right: Percentage of IgG1 + B cells; n = 5. (F) Different immunoglobulin isotypes in the supernatant were measured by multiplex assay; n = 5. Data in graphs represent mean ± SEM. Significance was tested by two-way ANOVA.

Techniques Used: Isolation, Cell Culture, Control, Expressing, Multiplex Assay

( A to G ) PBMCs from the patients with irAE were cultured in the plate coated with anti-CD3 and anti-CD28 (10 μg/ml) in the presence of IgG1 isotype control or anti–human IL-6R (50 μg/ml), anti–human IL-12p40 (50 μg/ml), and anti–human IFNAR1 (50 μg/ml) for 3 days; n = 9. (A) Expression of CD38 and CD127 on CD8 + T cells. Right: Percentage of CD38 + CD127 − CD8 + T cells. (B and C) CD8 + T cells activated for 5 days were restimulated with PMA, ionomycin, and monensin for 5 hours. (B) Expression of granzyme B and IFN-γ. Right: Percentage of granzyme B + IFN-γ + CD8 + T cells. (C) Expression of perforin and IFN-γ. Right: Percentage of perforin + IFN-γ + CD8 + T cells. [(D) and (E)] MFIs of GluCy5 (D), TMRM, and MTDR (E) in CD8 + T cells were presented. [(F) and (G)] CD4 + T cells activated for 5 days were restimulated with PMA, ionomycin, and monensin for 5 hours. (F) Expression of IL-21 and IL-2. Right: Percentage of IL-21 + IL-2 + CD4 + T cells. (G) Expression of CD38 and CXCR5 on CD4 + T cells. Right: Percentage of CD38 + CXCR5 − CD4 + T cells. Data in graphs represent mean ± SEM. Significance was tested paired Student’s t test [(A) to (G)].

Figure Legend Snippet: ( A to G ) PBMCs from the patients with irAE were cultured in the plate coated with anti-CD3 and anti-CD28 (10 μg/ml) in the presence of IgG1 isotype control or anti–human IL-6R (50 μg/ml), anti–human IL-12p40 (50 μg/ml), and anti–human IFNAR1 (50 μg/ml) for 3 days; n = 9. (A) Expression of CD38 and CD127 on CD8 + T cells. Right: Percentage of CD38 + CD127 − CD8 + T cells. (B and C) CD8 + T cells activated for 5 days were restimulated with PMA, ionomycin, and monensin for 5 hours. (B) Expression of granzyme B and IFN-γ. Right: Percentage of granzyme B + IFN-γ + CD8 + T cells. (C) Expression of perforin and IFN-γ. Right: Percentage of perforin + IFN-γ + CD8 + T cells. [(D) and (E)] MFIs of GluCy5 (D), TMRM, and MTDR (E) in CD8 + T cells were presented. [(F) and (G)] CD4 + T cells activated for 5 days were restimulated with PMA, ionomycin, and monensin for 5 hours. (F) Expression of IL-21 and IL-2. Right: Percentage of IL-21 + IL-2 + CD4 + T cells. (G) Expression of CD38 and CXCR5 on CD4 + T cells. Right: Percentage of CD38 + CXCR5 − CD4 + T cells. Data in graphs represent mean ± SEM. Significance was tested paired Student’s t test [(A) to (G)].

Techniques Used: Cell Culture, Control, Expressing

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( A ) Interleukin-2 (IL-2) and interferon gamma (IFN-γ) inhibition in CD3 + cells during allogeneic one-way MLR measured at day 2 and day 5, respectively, treated with 50 nM combination pharmacological inhibitors of TNF/TNFR targets of interest. Monotreatment groups included 50 nM of human IgG1. Cytokine inhibition was calculated as percent reduction from IgG1 control treatment. Ill denotes P <0.05 in student t-test for monotreatments vs. IgG1 control, # denotes P <0.05 in student t-tests for combination treatment groups vs. IgG1 controls and both constituent monotreatments. ( B ) Normalized IL-2 and IFN-γ expression in four promising combinations of TNF/TNFR inhibitors. ( C-D ) Proliferation in CD3 + cells during allogeneic one-way MLR measured at day 5 in the presence of combination pharmacological inhibition of TNF/TNFR targets of interest.* denotes P <0.05 in student t-test. Data from three unique stimulator-responder MLR pairs, mean ± SEM plotted. Large-molecule pharmacological TNF/TNFR inhibitors used: Adalimumab (abbr. Ada, α-TNF), Pateclizumab (α-LTA), Baminercept (abbr. Bam, LTβR decoy), Dapirolizumab (abbr. Dapiro, α-CD40L), Amlitelimab (abbr. Amlite, α-OX40L), CD30Li (α-CD30L), 4-1BB-Fc (4-1BB decoy), Quisovalimab (α-LIGHT), Duvakitug (α-TL1A), and GITRi (α-GITR).

Journal: bioRxiv

Article Title: Combination antagonism of TNF superfamily signaling for T cell immunosuppression

doi: 10.64898/2026.04.27.721101

Figure Lengend Snippet: ( A ) Interleukin-2 (IL-2) and interferon gamma (IFN-γ) inhibition in CD3 + cells during allogeneic one-way MLR measured at day 2 and day 5, respectively, treated with 50 nM combination pharmacological inhibitors of TNF/TNFR targets of interest. Monotreatment groups included 50 nM of human IgG1. Cytokine inhibition was calculated as percent reduction from IgG1 control treatment. Ill denotes P <0.05 in student t-test for monotreatments vs. IgG1 control, # denotes P <0.05 in student t-tests for combination treatment groups vs. IgG1 controls and both constituent monotreatments. ( B ) Normalized IL-2 and IFN-γ expression in four promising combinations of TNF/TNFR inhibitors. ( C-D ) Proliferation in CD3 + cells during allogeneic one-way MLR measured at day 5 in the presence of combination pharmacological inhibition of TNF/TNFR targets of interest.* denotes P <0.05 in student t-test. Data from three unique stimulator-responder MLR pairs, mean ± SEM plotted. Large-molecule pharmacological TNF/TNFR inhibitors used: Adalimumab (abbr. Ada, α-TNF), Pateclizumab (α-LTA), Baminercept (abbr. Bam, LTβR decoy), Dapirolizumab (abbr. Dapiro, α-CD40L), Amlitelimab (abbr. Amlite, α-OX40L), CD30Li (α-CD30L), 4-1BB-Fc (4-1BB decoy), Quisovalimab (α-LIGHT), Duvakitug (α-TL1A), and GITRi (α-GITR).

Article Snippet: Adalimumab (Cat. HY-P9908), Pateclizumab (Cat. HY-P990034), Baminercept (Cat. HY-P99459), Amlitelimab (Cat. HY-P99434), Dapirolizumab (Cat. HY-P99842A), Quisovalimab (Cat. HY-P99810), Duvakitug (Cat. HY-P99842A), human IgG1 (Cat. HY-P99001) and human IgG4 (Cat. HY-P99003) were purchased from MedChemExpress.

Techniques: Inhibition, Control, Expressing

( A-B ) Interleukin-2 (IL-2) and interferon gamma (IFN-γ) inhibition in CD3 + cells during allogeneic one-way MLR measured at day 2 and day 5, respectively, treated with 50 nM combination pharmacological inhibitors of TNF/TNFR targets of interest. Monotreatment groups included 50 nM of human IgG1. Cytokine expression normalized to IgG1 control treatment. * denotes P <0.05 in student t-test for monotreatments vs. IgG1 control. Data from three individual stimulator-responder MLR pairs, mean ± SEM plotted.

Journal: bioRxiv

Article Title: Combination antagonism of TNF superfamily signaling for T cell immunosuppression

doi: 10.64898/2026.04.27.721101

Figure Lengend Snippet: ( A-B ) Interleukin-2 (IL-2) and interferon gamma (IFN-γ) inhibition in CD3 + cells during allogeneic one-way MLR measured at day 2 and day 5, respectively, treated with 50 nM combination pharmacological inhibitors of TNF/TNFR targets of interest. Monotreatment groups included 50 nM of human IgG1. Cytokine expression normalized to IgG1 control treatment. * denotes P <0.05 in student t-test for monotreatments vs. IgG1 control. Data from three individual stimulator-responder MLR pairs, mean ± SEM plotted.

Techniques: Inhibition, Expressing, Control

Indirect immunofluorescence on sections of monkey retina. The fluorescence observed is identified by a black arrow. (A) Patient 4 (IgG4); (B) Patient 1 (IgG4); (C) Patient 3 (IgG1); (D) Patient 5 (IgG4); (E) Patient 2 (IgG1); (F) Patient 1 (IgG4) after immunoadsorption of IgLON5 antibodies; (G) Control with macular edema (IgG1); (H) Control with anti-Hu encephalitis (IgG1); (I) Control with CAR syndrome (IgG4). The different layers of the retina are identified by their initials: pigment epithelium (pe), photoreceptor layer (pr), outer grain layer (og), outer plexiform layer (op), inner grain layer (ig), inner plexiform layer (ip), ganglion cell layer (gc), nerve fibre layer (nf).

Journal: Journal of Translational Autoimmunity

Article Title: Anti-IgLON5 encephalitis is associated with anti-retinal immunological reactivity without retinal alteration

doi: 10.1016/j.jtauto.2026.100359

Figure Lengend Snippet: Indirect immunofluorescence on sections of monkey retina. The fluorescence observed is identified by a black arrow. (A) Patient 4 (IgG4); (B) Patient 1 (IgG4); (C) Patient 3 (IgG1); (D) Patient 5 (IgG4); (E) Patient 2 (IgG1); (F) Patient 1 (IgG4) after immunoadsorption of IgLON5 antibodies; (G) Control with macular edema (IgG1); (H) Control with anti-Hu encephalitis (IgG1); (I) Control with CAR syndrome (IgG4). The different layers of the retina are identified by their initials: pigment epithelium (pe), photoreceptor layer (pr), outer grain layer (og), outer plexiform layer (op), inner grain layer (ig), inner plexiform layer (ip), ganglion cell layer (gc), nerve fibre layer (nf).

Article Snippet: The reactivity of the patients’ sera and/or CSF against the retina was evaluated retrospectively with frozen samples (−80°, EXPLAINEUR biobank) through an indirect immunofluorescence technique using sections of monkey retina (Ref. FA1172-1005, Euroimmun), detected with an FITC-labelled secondary antibody anti-human IgAGM (Euroimmun conjugate) or directed against IgA (ref. F0204, DAKO), IgM (ref. F0203, DAKO), IgG1 (ref. 9052-02, Southern Biotech) and IgG4 (ref. 9200-02, Southern Biotech).

Techniques: Immunofluorescence, Fluorescence, Control

Journal: Science Advances

Article Title: Inflammatory arthritis irAE may represent a unique autoimmune disease primarily driven by T cells but likely not autoantibodies

doi: 10.1126/sciadv.aea4262

Figure Lengend Snippet: ( A ) Expression of CD27 and IgD on CD19 + B cells. Right: Percentage of IgD + CD27 − naïve B cells and IgD − CD27 − DN B cells. ( B ) Expression of CD27 and CD38 on CD19 + B cells. Right: Percentages of CD27 hi CD38 hi ASCs and CD27 + CD38 − memory B cells. ( C ) Expression of CD138 on CD27 hi CD38 hi ASCs. Right: Percentage of CD138 + ASCs and CD138 − ASCs. ( D ) Expression of CD11c and CD21 on CD19 + B cells. Right: Percentage of CD11c + CD21 − CD19 + B cells. [(A) to (D)] HC ( n = 63), irAE ( n = 33), RAC ( n = 46), and ICI ( n = 20). ( E to G ) GSEA was performed on the B cells between irAE and ICI. (E) Significantly enriched pathways in B cells from irAE and ICI. GSEA plots of IFN-α and IFN-γ response (F), and oxidative phosphorylation (G). ( H ) The volcano plots of the citrullinated or noncitrullinated relative IgG or IgM isotype autoantigen levels comparing RA versus HC, irAE versus ICI, irAE versus HC, or irAE versus RA. The autoantigens were labeled when P < 0.01. TNF-α reactivities resulted from the administration of anti–TNF-α therapy for the treatment of RA. ( I ) Immunoglobulin isotype levels in the plasma were measured by multiplex assay. HC ( n = 22), irAE ( n = 34), RAC ( n = 46), and ICI ( n = 26). ( J ) CXCL13 levels in the plasma were measured by enzyme-linked immunosorbent assay (ELISA). HC ( n = 20), irAE ( n = 34) RAC ( n = 47), and ICI ( n = 23). ( K ) B-cell activating factor (BAFF) levels in the plasma were measured by multiplex assay. HC ( n = 21), irAE ( n = 34), RAC ( n = 47), and ICI ( n = 18). Data in graphs represent mean ± SEM. Significance was tested by one-way ANOVA [(A) to (D) and (I) to (K)] and logistic regression (H). [(A) to (D) and (F) to (K)] ICI, ICI control.

Article Snippet: Pembrolizumab (100 μg/ml; Keytruda) or isotype control IgG4 (Bio X Cell, catalog no. CP147) was added into the culture media 2 days after stimulation, and B cells were further cultured for another 5 days.

Techniques: Expressing, Phospho-proteomics, Immunopeptidomics, Labeling, Clinical Proteomics, Multiplex Assay, Enzyme-linked Immunosorbent Assay, Control

Journal: Science Advances

Article Title: Inflammatory arthritis irAE may represent a unique autoimmune disease primarily driven by T cells but likely not autoantibodies

doi: 10.1126/sciadv.aea4262

Figure Lengend Snippet: ( A to C ) Human naïve B cells were isolated from PBMCs and cultured under indicated conditions for 7 days; pembrolizumab or isotype control IgG4 (IgG4 Iso) was added on day 2; n = 8. (A) Expression of CD38 and CD27 on B cells. Right: Percentages of CD27 + CD38 − and CD27 + CD38 + B cells. (B) Expression of CD138 on CD27 + CD38 + B cells. Right: Percentage of CD138 + CD27 + CD38 + B cells. (C) Different immunoglobulin isotypes were measured in the culture supernatant of (A) and (B) by multiplex assay. ( D to F ) B cells from Humanized PD-1 (HuPD-1) mice were isolated and cultured with LPS, IL-4, BAFF, or ODN 2006, anti-IgM, IL-21, IL-4 or R848, anti-IgM, anti-CD40, IL-21, and IFN-γ for 3 days; pembrolizumab or isotype control was added on day 1. (D) Expression of IgG2c on activated B cells. FSC-H, Forward scatter height. Right: Percentage of IgG2c + B cells; n = 5. (E) Expression of IgG1 on activated B cells. Right: Percentage of IgG1 + B cells; n = 5. (F) Different immunoglobulin isotypes in the supernatant were measured by multiplex assay; n = 5. Data in graphs represent mean ± SEM. Significance was tested by two-way ANOVA.

Techniques: Isolation, Cell Culture, Control, Expressing, Multiplex Assay

Journal: Science Advances

Article Title: Inflammatory arthritis irAE may represent a unique autoimmune disease primarily driven by T cells but likely not autoantibodies

doi: 10.1126/sciadv.aea4262

Figure Lengend Snippet: ( A to G ) PBMCs from the patients with irAE were cultured in the plate coated with anti-CD3 and anti-CD28 (10 μg/ml) in the presence of IgG1 isotype control or anti–human IL-6R (50 μg/ml), anti–human IL-12p40 (50 μg/ml), and anti–human IFNAR1 (50 μg/ml) for 3 days; n = 9. (A) Expression of CD38 and CD127 on CD8 + T cells. Right: Percentage of CD38 + CD127 − CD8 + T cells. (B and C) CD8 + T cells activated for 5 days were restimulated with PMA, ionomycin, and monensin for 5 hours. (B) Expression of granzyme B and IFN-γ. Right: Percentage of granzyme B + IFN-γ + CD8 + T cells. (C) Expression of perforin and IFN-γ. Right: Percentage of perforin + IFN-γ + CD8 + T cells. [(D) and (E)] MFIs of GluCy5 (D), TMRM, and MTDR (E) in CD8 + T cells were presented. [(F) and (G)] CD4 + T cells activated for 5 days were restimulated with PMA, ionomycin, and monensin for 5 hours. (F) Expression of IL-21 and IL-2. Right: Percentage of IL-21 + IL-2 + CD4 + T cells. (G) Expression of CD38 and CXCR5 on CD4 + T cells. Right: Percentage of CD38 + CXCR5 − CD4 + T cells. Data in graphs represent mean ± SEM. Significance was tested paired Student’s t test [(A) to (G)].

Techniques: Cell Culture, Control, Expressing

Spatial distribution of immunoglobulins in human atherosclerotic plaques. ( A ) Representative formalin-fixed paraffin-embedded (FFPE) carotid plaque sections stained for IgA, IgE, IgM, and IgG, with quantification of total antibody-positive area per plaque. ( B ) Regional analysis of antibody staining in core, shoulder, and fibrous cap compartments (repeated-measures one-way ANOVA with Tukey’s post hoc test; n = 8 plaques). ( C ) Representative CD79A staining highlighting intraplaque B cells, with frequency of B-cell detection across samples. Data are presented as mean ± SD and scale bars as indicated.

Journal: bioRxiv

Article Title: Antibody recycling via FcRn drives atherosclerotic plaque vulnerability

doi: 10.64898/2026.03.08.710352

Figure Lengend Snippet: Spatial distribution of immunoglobulins in human atherosclerotic plaques. ( A ) Representative formalin-fixed paraffin-embedded (FFPE) carotid plaque sections stained for IgA, IgE, IgM, and IgG, with quantification of total antibody-positive area per plaque. ( B ) Regional analysis of antibody staining in core, shoulder, and fibrous cap compartments (repeated-measures one-way ANOVA with Tukey’s post hoc test; n = 8 plaques). ( C ) Representative CD79A staining highlighting intraplaque B cells, with frequency of B-cell detection across samples. Data are presented as mean ± SD and scale bars as indicated.

Article Snippet: Cells were treated with 10 μg/ml rozanolixizumab (anti-human FcRn; HY-P9979, MedChemExpress) or an IgG4 isotype control (HY-P99003, MedChemExpress).

Techniques: Formalin-fixed Paraffin-Embedded, Staining

Local IgG deposition associates with markers of atherosclerotic plaque vulnerability. ( A ) Heatmap showing correlations between IgG staining and morphological features of plaque vulnerability; Spearman r-values are displayed for significant correlations. ( B ) Representative micrographs illustrating the assessed morphological features. ( C ) Stratification of plaques into IgG-poor (<33% IgG⁺ area) and IgG-rich (>33% IgG⁺ area) groups. ( D ) Representative cap-region micrographs from IgG-poor and IgG-rich plaques; colored arrows indicate cap structure, and black arrows denote measured cap thickness. ( E ) Quantification of collagen content, cap thickness, and vulnerability index in IgG-rich versus IgG-poor plaques (unpaired t- test). ( F ) Computer tomography-based quantification of lipid-rich necrotic core, minimal cap thickness, and vulnerability index in IgG-rich versus IgG-poor plaques (Mann-Whitney test). Data are presented as mean ± SD and scale bars as indicated.

Journal: bioRxiv

Article Title: Antibody recycling via FcRn drives atherosclerotic plaque vulnerability

doi: 10.64898/2026.03.08.710352

Figure Lengend Snippet: Local IgG deposition associates with markers of atherosclerotic plaque vulnerability. ( A ) Heatmap showing correlations between IgG staining and morphological features of plaque vulnerability; Spearman r-values are displayed for significant correlations. ( B ) Representative micrographs illustrating the assessed morphological features. ( C ) Stratification of plaques into IgG-poor (<33% IgG⁺ area) and IgG-rich (>33% IgG⁺ area) groups. ( D ) Representative cap-region micrographs from IgG-poor and IgG-rich plaques; colored arrows indicate cap structure, and black arrows denote measured cap thickness. ( E ) Quantification of collagen content, cap thickness, and vulnerability index in IgG-rich versus IgG-poor plaques (unpaired t- test). ( F ) Computer tomography-based quantification of lipid-rich necrotic core, minimal cap thickness, and vulnerability index in IgG-rich versus IgG-poor plaques (Mann-Whitney test). Data are presented as mean ± SD and scale bars as indicated.

Article Snippet: Cells were treated with 10 μg/ml rozanolixizumab (anti-human FcRn; HY-P9979, MedChemExpress) or an IgG4 isotype control (HY-P99003, MedChemExpress).

Techniques: Staining, Tomography, MANN-WHITNEY

Dynamic accumulation of apoB-specific IgG in human atherosclerotic plaques. ( A ) Associations between immunoglobulin concentrations and apoB levels in carotid plaque protein extracts. ( B ) Anti-apoB IgG levels measured in paired plasma and plaque samples normalized to 1 µg/ml total IgG (paired t -test). ( C ) Plaque anti-apoB IgG levels in asymptomatic versus symptomatic patients (unpaired t -test). ( D ) Schematic illustration of apoB, anti-apoB IgG, and apoB-IgG immune complexes. ( E ) Plaque apoB concentrations (unpaired t -test). ( F ) Levels of apoB-IgG immune complexes in plaques (unpaired t- test). ( G ) Matrix illustrating relationships among these parameters in asymptomatic (lower left) and symptomatic (upper right) patients. RLU, relative light units. Data are presented as mean ± SD.

Journal: bioRxiv

Article Title: Antibody recycling via FcRn drives atherosclerotic plaque vulnerability

doi: 10.64898/2026.03.08.710352

Figure Lengend Snippet: Dynamic accumulation of apoB-specific IgG in human atherosclerotic plaques. ( A ) Associations between immunoglobulin concentrations and apoB levels in carotid plaque protein extracts. ( B ) Anti-apoB IgG levels measured in paired plasma and plaque samples normalized to 1 µg/ml total IgG (paired t -test). ( C ) Plaque anti-apoB IgG levels in asymptomatic versus symptomatic patients (unpaired t -test). ( D ) Schematic illustration of apoB, anti-apoB IgG, and apoB-IgG immune complexes. ( E ) Plaque apoB concentrations (unpaired t -test). ( F ) Levels of apoB-IgG immune complexes in plaques (unpaired t- test). ( G ) Matrix illustrating relationships among these parameters in asymptomatic (lower left) and symptomatic (upper right) patients. RLU, relative light units. Data are presented as mean ± SD.

Article Snippet: Cells were treated with 10 μg/ml rozanolixizumab (anti-human FcRn; HY-P9979, MedChemExpress) or an IgG4 isotype control (HY-P99003, MedChemExpress).

Techniques: Clinical Proteomics

Expression of the IgG recycling receptor FcRn in plaque macrophages. ( A ) FCGRT expression in carotid plaques compared with non-diseased iliac arteries (unpaired t -test). Data are presented with median levels indicated. ( B ) Immunofluorescence staining of FcRn and CD163⁺ macrophages in the shoulder region of a carotid plaque. ( C ) Integrated single-cell RNA-seq analysis of myeloid populations in human atherosclerosis with a feature plot showing FCGRT expression (n = 26). ( D ) Age distribution in the carotid stenosis cohort and Spearman correlations between macrophage subset markers and patient age. Mac, macrophage; cDC, conventional dendritic cell; infla, inflammatory.

Journal: bioRxiv

Article Title: Antibody recycling via FcRn drives atherosclerotic plaque vulnerability

doi: 10.64898/2026.03.08.710352

Figure Lengend Snippet: Expression of the IgG recycling receptor FcRn in plaque macrophages. ( A ) FCGRT expression in carotid plaques compared with non-diseased iliac arteries (unpaired t -test). Data are presented with median levels indicated. ( B ) Immunofluorescence staining of FcRn and CD163⁺ macrophages in the shoulder region of a carotid plaque. ( C ) Integrated single-cell RNA-seq analysis of myeloid populations in human atherosclerosis with a feature plot showing FCGRT expression (n = 26). ( D ) Age distribution in the carotid stenosis cohort and Spearman correlations between macrophage subset markers and patient age. Mac, macrophage; cDC, conventional dendritic cell; infla, inflammatory.

Article Snippet: Cells were treated with 10 μg/ml rozanolixizumab (anti-human FcRn; HY-P9979, MedChemExpress) or an IgG4 isotype control (HY-P99003, MedChemExpress).

Techniques: Expressing, Immunofluorescence, Staining, Single Cell, RNA Sequencing

FcRn blockade or knockdown suppresses IgG recycling and inflammatory activation in macrophages. ( A ) Formation of LDL-IgG immune complexes in vitro using mouse IgG reactive against LDL. ( B ) Effects of Fcgrt knockdown in RAW 264.7 macrophages on IgG recycling and cytokine secretion, along with uptake of fluorescently labeled LDL (one-way ANOVA with Holm-Šídák correction). ( C ) Schematic of the THP-1 macrophage system used to assess the impact of rozanolixizumab on FcRn-dependent handling of immune complexes formed with plaque-derived IgG. ( D ) FcRn blockade reduces IgG1 recycling, TNF secretion, and alters uptake of fluorescently labeled LDL in THP-1 macrophages (one-way ANOVA with Holm-Šídák correction). MFI, mean fluorescence intensity; RQ, relative quantification. Data are presented with mean levels indicated.

Journal: bioRxiv

Article Title: Antibody recycling via FcRn drives atherosclerotic plaque vulnerability

doi: 10.64898/2026.03.08.710352

Figure Lengend Snippet: FcRn blockade or knockdown suppresses IgG recycling and inflammatory activation in macrophages. ( A ) Formation of LDL-IgG immune complexes in vitro using mouse IgG reactive against LDL. ( B ) Effects of Fcgrt knockdown in RAW 264.7 macrophages on IgG recycling and cytokine secretion, along with uptake of fluorescently labeled LDL (one-way ANOVA with Holm-Šídák correction). ( C ) Schematic of the THP-1 macrophage system used to assess the impact of rozanolixizumab on FcRn-dependent handling of immune complexes formed with plaque-derived IgG. ( D ) FcRn blockade reduces IgG1 recycling, TNF secretion, and alters uptake of fluorescently labeled LDL in THP-1 macrophages (one-way ANOVA with Holm-Šídák correction). MFI, mean fluorescence intensity; RQ, relative quantification. Data are presented with mean levels indicated.

Article Snippet: Cells were treated with 10 μg/ml rozanolixizumab (anti-human FcRn; HY-P9979, MedChemExpress) or an IgG4 isotype control (HY-P99003, MedChemExpress).

Techniques: Knockdown, Activation Assay, In Vitro, Labeling, Derivative Assay, Fluorescence, Quantitative Proteomics

FcRn-dependent IgG recycling promotes MMP-9 production in macrophages and human plaques. ( B ) Silencing Fcgrt reduces MMP-9 production in RAW 264.7 macrophages stimulated with LDL immune complexes (unpaired t -test). ( C ) FcRn blockade with rozanolixizumab lowers MMP-9 production in LDL immune complex-stimulated THP-1 macrophages (unpaired t -test). ( D ) MMP-9 levels positively correlate with antibody concentrations in carotid plaques; Spearman r-values are shown for significant associations. ( E ) FCGRT transcript levels correlate with markers of plaque stability and vulnerability in carotid plaque tissue. ( F ) Ex vivo stimulation of human carotid plaques for 24 hours: IgG and MMP-9 were measured in plaque extracts, and TNF was quantified in supernatants (ratio paired t -test). AU, arbitrary units; RQ, relative quantification; AS, asymptomatic; S, symptomatic. Data are presented as mean ± SD.

Journal: bioRxiv

Article Title: Antibody recycling via FcRn drives atherosclerotic plaque vulnerability

doi: 10.64898/2026.03.08.710352

Figure Lengend Snippet: FcRn-dependent IgG recycling promotes MMP-9 production in macrophages and human plaques. ( B ) Silencing Fcgrt reduces MMP-9 production in RAW 264.7 macrophages stimulated with LDL immune complexes (unpaired t -test). ( C ) FcRn blockade with rozanolixizumab lowers MMP-9 production in LDL immune complex-stimulated THP-1 macrophages (unpaired t -test). ( D ) MMP-9 levels positively correlate with antibody concentrations in carotid plaques; Spearman r-values are shown for significant associations. ( E ) FCGRT transcript levels correlate with markers of plaque stability and vulnerability in carotid plaque tissue. ( F ) Ex vivo stimulation of human carotid plaques for 24 hours: IgG and MMP-9 were measured in plaque extracts, and TNF was quantified in supernatants (ratio paired t -test). AU, arbitrary units; RQ, relative quantification; AS, asymptomatic; S, symptomatic. Data are presented as mean ± SD.

Article Snippet: Cells were treated with 10 μg/ml rozanolixizumab (anti-human FcRn; HY-P9979, MedChemExpress) or an IgG4 isotype control (HY-P99003, MedChemExpress).

Techniques: Ex Vivo, Quantitative Proteomics

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