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anti human c1q fitc mab  (Bio-Rad)


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    Structured Review

    Bio-Rad anti human c1q fitc mab
    Binding of neutrophils autoantibodies to target antigens expressed on neutrophil fails to fix complement. Complement fixing capacities of human IgG from transfusion‐related acute lung injury (TRALI) sera with neutrophil autoantibodies were evaluated in flow cytometry. Isolated neutrophils (2 × 10 5 ) were incubated with human sera in presence of human <t>C1q</t> protein for 30 min. After washing, bound C1q protein was detected by fluorescein isothiocyanate (FITC)‐labeled anti‐human C1q antibody in flowcytometry. Control serum and serum containing complement fixing alloantibodies served as negative and positive controls, respectively Data are shown as means ± SEM for four separate donors. ** p < 0.01.
    Anti Human C1q Fitc Mab, supplied by Bio-Rad, used in various techniques. Bioz Stars score: 93/100, based on 39 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/sheep+monoclonal+antibodies/Sheep+anti+Human+C1q/pmc13049269-41-76-80
    Average 93 stars, based on 39 article reviews
    anti human c1q fitc mab - by Bioz Stars, 2026-09
    93/100 stars

    Images

    1) Product Images from "Neutrophil‐reactive autoantibodies in blood donors: Can we expect TRALI ?"

    Article Title: Neutrophil‐reactive autoantibodies in blood donors: Can we expect TRALI ?

    Journal: Transfusion

    doi: 10.1111/trf.70125

    Binding of neutrophils autoantibodies to target antigens expressed on neutrophil fails to fix complement. Complement fixing capacities of human IgG from transfusion‐related acute lung injury (TRALI) sera with neutrophil autoantibodies were evaluated in flow cytometry. Isolated neutrophils (2 × 10 5 ) were incubated with human sera in presence of human C1q protein for 30 min. After washing, bound C1q protein was detected by fluorescein isothiocyanate (FITC)‐labeled anti‐human C1q antibody in flowcytometry. Control serum and serum containing complement fixing alloantibodies served as negative and positive controls, respectively Data are shown as means ± SEM for four separate donors. ** p < 0.01.
    Figure Legend Snippet: Binding of neutrophils autoantibodies to target antigens expressed on neutrophil fails to fix complement. Complement fixing capacities of human IgG from transfusion‐related acute lung injury (TRALI) sera with neutrophil autoantibodies were evaluated in flow cytometry. Isolated neutrophils (2 × 10 5 ) were incubated with human sera in presence of human C1q protein for 30 min. After washing, bound C1q protein was detected by fluorescein isothiocyanate (FITC)‐labeled anti‐human C1q antibody in flowcytometry. Control serum and serum containing complement fixing alloantibodies served as negative and positive controls, respectively Data are shown as means ± SEM for four separate donors. ** p < 0.01.

    Techniques Used: Binding Assay, Flow Cytometry, Isolation, Incubation, Labeling, Control

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    Concentration Assay:

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    Enzyme-linked Immunosorbent Assay:

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    Clinical Proteomics:

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    Cell Culture:

    Article Title: Fetal microglial phenotype in vitro carries memory of prior in vivo exposure to inflammation.
    Article Snippet: .. Briefly, 96-well plates (Nunc Maxisorp, high capacity microtitre wells) were pre-coated with the capture antibody, the mouse anti sheep monoclonal antibodies (IL-6, MCA1659; IL-1β, MCA1658, Bio Rad AbD Serotec) at a concentration 4μg/ml on ELISA plates at 4◦C for overnight, after 3 times wash with washing buffer (0.05% Tween 20 in PBS, PBST), plates were then blocked for 1 h with 1% BSA in PBST for plasma samples or 10% FBS for cell culture media. ..

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    Saline:

    Article Title: Can Monitoring Fetal Intestinal Inflammation Using Heart Rate Variability Analysis Signal Incipient Necrotizing Enterocolitis of the Neonate?
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    90
    Fapon Biotech hydrocortisone sheep-derived monoclonal antibody cort-reab-c1-001
    (A) Anti-CRB2 IgG and <t>anti-Nephrin</t> IgG titers in sera of patients with non-biopsied idiopathic nephrotic syndrome (INS, N child = 21), including steroid-sensitive (SSNS, N child = 20) and steroid-resistant (SRNS, N child = 1), or the histological diagnoses of minimal change disease (MCD, N child = 22, N adult = 10), primary focal segmental glomerulosclerosis (FSGS, N child = 8, N adult = 21), and membranous nephropathy (MN, N child = 2, N adult = 6), or other glomerular diseases (Other GN, N child = 2, N adult = 12) as determined by quantitative ELISA. The dotted line shows a threshold for seropositivity determined using healthy control (HC, N child = 7, N adult = 21) sera. The y-axis for anti-Nephrin titers is split to enhance visibility of values near the threshold. (B) Anti-CRB2 IgG and anti-Nephrin IgG titers for idiopathic podocytopathies divided by steroid responsiveness. (C) Anti-CRB2 IgG and anti-Nephrin IgG titers are compared between children and adults with idiopathic podocytopathies (SSNS, SRNS, MCD, and FSGS). (D) Correlations between anti-CRB2 IgG and anti-Nephrin IgG titers in children and adults with idiopathic podocytopathies. (E) Changes in anti-CRB2 IgG and anti-Nephrin IgG titers during active disease and remission in children ( N = 24) and adults ( N = 9) with idiopathic podocytopathies. (F) Representative glomeruli from flash frozen kidney biopsies from anti-CRB2 IgG seropositive and seronegative patients with idiopathic podocytopathies showing CRB2 (green) and IgG (red) co-localization. (G) Average IgG staining intensity across all glomeruli are compared between anti-CRB2 IgG seropositive ( N = 5) and seronegative ( N = 2) individuals. (H) Representative glomerulus from a single patient with both anti-CRB2 and anti-Nephrin IgG showing CRB2 (magenta) and IgG (green) or Nephrin (red) and IgG (green) co-localization visualized with high-resolution structured illumination microscopy. (I) Overlap between IgG and Nephrin, IgG and CRB2, and Nephrin and CRB2 calculated using the Mander’s coefficient across three different areas of two glomeruli from the patient in H. (J) Schematic showing mouse immunization and re-challenge schedule for induction of experimental autoimmune nephrotic syndrome. (K) Urinary albumin-to-creatinine ratios (uACR) from immunized mice at 6-weeks and 12-weeks following immunization determined using quantitative ELISAs. (L) Anti-CRB2 IgG and anti-Nephrin IgG titers in immunized mice. In all graphs, each dot represents a single patient or mouse, except in J where they represent distinct regions of a glomerulus. Summary statistics are expressed as a median with 95% confidence intervals in A-C, G, I or mean with standard deviation in K and L. P -values were determined using Kruskal-Wallis tests with Dunn’s correction for multiple comparisons in B and I, Mann-Whitney U -tests in C, one-way ANOVA with Tukey’s correction for multiple testing in K and L, and Wilcoxon matched-paired signed rank test in E.
    Hydrocortisone Sheep Derived Monoclonal Antibody Cort Reab C1 001, supplied by Fapon Biotech, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/sheep+monoclonal+antibodies/hydrocortisone+sheep+derived+monoclonal+antibody+cort+reab+c1+001/pm40565714-50-0-22
    Average 90 stars, based on 1 article reviews
    hydrocortisone sheep-derived monoclonal antibody cort-reab-c1-001 - by Bioz Stars, 2026-09
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    96
    Bio-Rad ahp500gt rrid ab 2203291 rabbit monoclonal
    (A) Anti-CRB2 IgG and <t>anti-Nephrin</t> IgG titers in sera of patients with non-biopsied idiopathic nephrotic syndrome (INS, N child = 21), including steroid-sensitive (SSNS, N child = 20) and steroid-resistant (SRNS, N child = 1), or the histological diagnoses of minimal change disease (MCD, N child = 22, N adult = 10), primary focal segmental glomerulosclerosis (FSGS, N child = 8, N adult = 21), and membranous nephropathy (MN, N child = 2, N adult = 6), or other glomerular diseases (Other GN, N child = 2, N adult = 12) as determined by quantitative ELISA. The dotted line shows a threshold for seropositivity determined using healthy control (HC, N child = 7, N adult = 21) sera. The y-axis for anti-Nephrin titers is split to enhance visibility of values near the threshold. (B) Anti-CRB2 IgG and anti-Nephrin IgG titers for idiopathic podocytopathies divided by steroid responsiveness. (C) Anti-CRB2 IgG and anti-Nephrin IgG titers are compared between children and adults with idiopathic podocytopathies (SSNS, SRNS, MCD, and FSGS). (D) Correlations between anti-CRB2 IgG and anti-Nephrin IgG titers in children and adults with idiopathic podocytopathies. (E) Changes in anti-CRB2 IgG and anti-Nephrin IgG titers during active disease and remission in children ( N = 24) and adults ( N = 9) with idiopathic podocytopathies. (F) Representative glomeruli from flash frozen kidney biopsies from anti-CRB2 IgG seropositive and seronegative patients with idiopathic podocytopathies showing CRB2 (green) and IgG (red) co-localization. (G) Average IgG staining intensity across all glomeruli are compared between anti-CRB2 IgG seropositive ( N = 5) and seronegative ( N = 2) individuals. (H) Representative glomerulus from a single patient with both anti-CRB2 and anti-Nephrin IgG showing CRB2 (magenta) and IgG (green) or Nephrin (red) and IgG (green) co-localization visualized with high-resolution structured illumination microscopy. (I) Overlap between IgG and Nephrin, IgG and CRB2, and Nephrin and CRB2 calculated using the Mander’s coefficient across three different areas of two glomeruli from the patient in H. (J) Schematic showing mouse immunization and re-challenge schedule for induction of experimental autoimmune nephrotic syndrome. (K) Urinary albumin-to-creatinine ratios (uACR) from immunized mice at 6-weeks and 12-weeks following immunization determined using quantitative ELISAs. (L) Anti-CRB2 IgG and anti-Nephrin IgG titers in immunized mice. In all graphs, each dot represents a single patient or mouse, except in J where they represent distinct regions of a glomerulus. Summary statistics are expressed as a median with 95% confidence intervals in A-C, G, I or mean with standard deviation in K and L. P -values were determined using Kruskal-Wallis tests with Dunn’s correction for multiple comparisons in B and I, Mann-Whitney U -tests in C, one-way ANOVA with Tukey’s correction for multiple testing in K and L, and Wilcoxon matched-paired signed rank test in E.
    Ahp500gt Rrid Ab 2203291 Rabbit Monoclonal, supplied by Bio-Rad, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/sheep+monoclonal+antibodies/Sheep+anti+Human+TGN46/pm40439270-73-120-118
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    ahp500gt rrid ab 2203291 rabbit monoclonal - by Bioz Stars, 2026-09
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    Image Search Results


    Binding of neutrophils autoantibodies to target antigens expressed on neutrophil fails to fix complement. Complement fixing capacities of human IgG from transfusion‐related acute lung injury (TRALI) sera with neutrophil autoantibodies were evaluated in flow cytometry. Isolated neutrophils (2 × 10 5 ) were incubated with human sera in presence of human C1q protein for 30 min. After washing, bound C1q protein was detected by fluorescein isothiocyanate (FITC)‐labeled anti‐human C1q antibody in flowcytometry. Control serum and serum containing complement fixing alloantibodies served as negative and positive controls, respectively Data are shown as means ± SEM for four separate donors. ** p < 0.01.

    Journal: Transfusion

    Article Title: Neutrophil‐reactive autoantibodies in blood donors: Can we expect TRALI ?

    doi: 10.1111/trf.70125

    Figure Lengend Snippet: Binding of neutrophils autoantibodies to target antigens expressed on neutrophil fails to fix complement. Complement fixing capacities of human IgG from transfusion‐related acute lung injury (TRALI) sera with neutrophil autoantibodies were evaluated in flow cytometry. Isolated neutrophils (2 × 10 5 ) were incubated with human sera in presence of human C1q protein for 30 min. After washing, bound C1q protein was detected by fluorescein isothiocyanate (FITC)‐labeled anti‐human C1q antibody in flowcytometry. Control serum and serum containing complement fixing alloantibodies served as negative and positive controls, respectively Data are shown as means ± SEM for four separate donors. ** p < 0.01.

    Article Snippet: Anti‐CD177 (clone MEM‐166, Serotec, Duesseldorf, Germany), anti‐CD11a (clone B‐B15, Medix Biochemica, Konstanz, Germany), anti‐CD11b (clone Mac‐1, Beckman Coulter, Krefeld, Germany), anti‐CD18 (clone ITGB2, Biozol Diagnostica, Hamburg, Germany), anti‐CD16b (clone LNK16, Santa Cruz Biotechnology, Heidelberg, Germany; clone 3G8, Beckman Coulter, Krefeld, Germany) and anti‐HLA class I (clone W6/32, Biolegend, Koblenz, Germany); ortho ‐pheneylendiamine (Dako, Hamburg, Germany); lymphocyte separation media (Anprotec, Bruckberg, Germany); CM‐H 2 DCFDA (Thermofisher, Darmstadt, Germany); human C1q complement protein (Merck, Darmstadt, Germany); polyclonal sheep anti‐human C1q FITC mAb (Bio‐Rad, Dreieich, Germany); fluorescein‐isothiocyanate‐labeled bovine serum albumin (FITC‐BSA, Taufkirchen, Germany); fibronectin (Merck, Darmstadt, Germany); FITC‐labeled rabbit anti‐human IgG antibody (Jackson ImmunoResources, Brussels, Belgium); Phorbol 12‐myristate 13‐acetate (Merck, Darmstadt, Germany); paraformaldehyde (PFA) (Carl Roth, Karlsruhe Germany); Dulbecco's Modified Eagle Medium (DMEM) (Anprotec, Bruckberg, Germany); and EBM‐2 bullet kit (Lonza, Cologne, Germany).

    Techniques: Binding Assay, Flow Cytometry, Isolation, Incubation, Labeling, Control

    (A) Anti-CRB2 IgG and anti-Nephrin IgG titers in sera of patients with non-biopsied idiopathic nephrotic syndrome (INS, N child = 21), including steroid-sensitive (SSNS, N child = 20) and steroid-resistant (SRNS, N child = 1), or the histological diagnoses of minimal change disease (MCD, N child = 22, N adult = 10), primary focal segmental glomerulosclerosis (FSGS, N child = 8, N adult = 21), and membranous nephropathy (MN, N child = 2, N adult = 6), or other glomerular diseases (Other GN, N child = 2, N adult = 12) as determined by quantitative ELISA. The dotted line shows a threshold for seropositivity determined using healthy control (HC, N child = 7, N adult = 21) sera. The y-axis for anti-Nephrin titers is split to enhance visibility of values near the threshold. (B) Anti-CRB2 IgG and anti-Nephrin IgG titers for idiopathic podocytopathies divided by steroid responsiveness. (C) Anti-CRB2 IgG and anti-Nephrin IgG titers are compared between children and adults with idiopathic podocytopathies (SSNS, SRNS, MCD, and FSGS). (D) Correlations between anti-CRB2 IgG and anti-Nephrin IgG titers in children and adults with idiopathic podocytopathies. (E) Changes in anti-CRB2 IgG and anti-Nephrin IgG titers during active disease and remission in children ( N = 24) and adults ( N = 9) with idiopathic podocytopathies. (F) Representative glomeruli from flash frozen kidney biopsies from anti-CRB2 IgG seropositive and seronegative patients with idiopathic podocytopathies showing CRB2 (green) and IgG (red) co-localization. (G) Average IgG staining intensity across all glomeruli are compared between anti-CRB2 IgG seropositive ( N = 5) and seronegative ( N = 2) individuals. (H) Representative glomerulus from a single patient with both anti-CRB2 and anti-Nephrin IgG showing CRB2 (magenta) and IgG (green) or Nephrin (red) and IgG (green) co-localization visualized with high-resolution structured illumination microscopy. (I) Overlap between IgG and Nephrin, IgG and CRB2, and Nephrin and CRB2 calculated using the Mander’s coefficient across three different areas of two glomeruli from the patient in H. (J) Schematic showing mouse immunization and re-challenge schedule for induction of experimental autoimmune nephrotic syndrome. (K) Urinary albumin-to-creatinine ratios (uACR) from immunized mice at 6-weeks and 12-weeks following immunization determined using quantitative ELISAs. (L) Anti-CRB2 IgG and anti-Nephrin IgG titers in immunized mice. In all graphs, each dot represents a single patient or mouse, except in J where they represent distinct regions of a glomerulus. Summary statistics are expressed as a median with 95% confidence intervals in A-C, G, I or mean with standard deviation in K and L. P -values were determined using Kruskal-Wallis tests with Dunn’s correction for multiple comparisons in B and I, Mann-Whitney U -tests in C, one-way ANOVA with Tukey’s correction for multiple testing in K and L, and Wilcoxon matched-paired signed rank test in E.

    Journal: bioRxiv

    Article Title: Autoantibodies targeting CRB2 and Nephrin correlate with extrafollicular B cells in idiopathic podocytopathies

    doi: 10.1101/2025.09.06.674608

    Figure Lengend Snippet: (A) Anti-CRB2 IgG and anti-Nephrin IgG titers in sera of patients with non-biopsied idiopathic nephrotic syndrome (INS, N child = 21), including steroid-sensitive (SSNS, N child = 20) and steroid-resistant (SRNS, N child = 1), or the histological diagnoses of minimal change disease (MCD, N child = 22, N adult = 10), primary focal segmental glomerulosclerosis (FSGS, N child = 8, N adult = 21), and membranous nephropathy (MN, N child = 2, N adult = 6), or other glomerular diseases (Other GN, N child = 2, N adult = 12) as determined by quantitative ELISA. The dotted line shows a threshold for seropositivity determined using healthy control (HC, N child = 7, N adult = 21) sera. The y-axis for anti-Nephrin titers is split to enhance visibility of values near the threshold. (B) Anti-CRB2 IgG and anti-Nephrin IgG titers for idiopathic podocytopathies divided by steroid responsiveness. (C) Anti-CRB2 IgG and anti-Nephrin IgG titers are compared between children and adults with idiopathic podocytopathies (SSNS, SRNS, MCD, and FSGS). (D) Correlations between anti-CRB2 IgG and anti-Nephrin IgG titers in children and adults with idiopathic podocytopathies. (E) Changes in anti-CRB2 IgG and anti-Nephrin IgG titers during active disease and remission in children ( N = 24) and adults ( N = 9) with idiopathic podocytopathies. (F) Representative glomeruli from flash frozen kidney biopsies from anti-CRB2 IgG seropositive and seronegative patients with idiopathic podocytopathies showing CRB2 (green) and IgG (red) co-localization. (G) Average IgG staining intensity across all glomeruli are compared between anti-CRB2 IgG seropositive ( N = 5) and seronegative ( N = 2) individuals. (H) Representative glomerulus from a single patient with both anti-CRB2 and anti-Nephrin IgG showing CRB2 (magenta) and IgG (green) or Nephrin (red) and IgG (green) co-localization visualized with high-resolution structured illumination microscopy. (I) Overlap between IgG and Nephrin, IgG and CRB2, and Nephrin and CRB2 calculated using the Mander’s coefficient across three different areas of two glomeruli from the patient in H. (J) Schematic showing mouse immunization and re-challenge schedule for induction of experimental autoimmune nephrotic syndrome. (K) Urinary albumin-to-creatinine ratios (uACR) from immunized mice at 6-weeks and 12-weeks following immunization determined using quantitative ELISAs. (L) Anti-CRB2 IgG and anti-Nephrin IgG titers in immunized mice. In all graphs, each dot represents a single patient or mouse, except in J where they represent distinct regions of a glomerulus. Summary statistics are expressed as a median with 95% confidence intervals in A-C, G, I or mean with standard deviation in K and L. P -values were determined using Kruskal-Wallis tests with Dunn’s correction for multiple comparisons in B and I, Mann-Whitney U -tests in C, one-way ANOVA with Tukey’s correction for multiple testing in K and L, and Wilcoxon matched-paired signed rank test in E.

    Article Snippet: The standard curve was generated using seven serial dilutions of polyclonal rabbit anti-human CRB2 antibody (custom produced by MediMabs, Montreal, using human CRB2 597- 943 recombinant protein) or monoclonal sheep anti-human Nephrin antibody (RnD systems).

    Techniques: Enzyme-linked Immunosorbent Assay, Control, Staining, Microscopy, Standard Deviation, MANN-WHITNEY

    (A) Timeline of autoantibody seropositivity status and proteinuria severity measured with the protein-to-creatinine ratio (uPCR in g/g) in patients with samples available at three or more independent clinical visits. (B) Upset plot showing overall seropositivity for IgG, IgM and IgA isotypes for anti-CRB2 (in blue) and anti-Nephrin (in green) autoantibodies for children (left) and adults (right). For each subgroup, vertical histograms show the number of patients seropositive for each isotype combination while horizontal histograms show the total number of patients seropositive for each isotype. (C) Proportion of patients with disease onset in childhood or adulthood stratified by autoantibody seropositivity. The size of each pie chart is proportional to the number of individuals captured in that group. Forest plots of the relative risk for adulthood onset given anti-CRB2 or anti-Nephrin seropositivity is plotted below the pie charts. (D) Correlation of uPCR and IgG autoantibody titers in patients with non-biopsied idiopathic nephrotic syndrome (INS, N child = 18), including steroid-sensitive (SSNS, N child = 17) and steroid-resistant (SRNS, N child = 1), or the histological diagnoses of minimal change disease (MCD, N child = 19, N adult = 10) and primary focal segmental glomerulosclerosis (FSGS, N child = 6, N adult = 18). (E) Comparison of uPCR in autoantibody seropositive or seronegative donors shown for the total cohort or for children and adults independently. (F) Representative glomeruli from flash frozen kidney biopsies from the remaining four anti-CRB2 IgG seropositive patients and one seronegative patient present in the quantification in showing CRB2 (green) and IgG (red) co-localization. In D and E, each dot represents a single donor, and summary statistics are shown as median with 95% confidence intervals. P -values were determined using Fisher’s exact tests in C, non-parametric Spearman correlation in D, and Mann-Whitney U -tests in E. This Supplemental Figure is associated with .

    Journal: bioRxiv

    Article Title: Autoantibodies targeting CRB2 and Nephrin correlate with extrafollicular B cells in idiopathic podocytopathies

    doi: 10.1101/2025.09.06.674608

    Figure Lengend Snippet: (A) Timeline of autoantibody seropositivity status and proteinuria severity measured with the protein-to-creatinine ratio (uPCR in g/g) in patients with samples available at three or more independent clinical visits. (B) Upset plot showing overall seropositivity for IgG, IgM and IgA isotypes for anti-CRB2 (in blue) and anti-Nephrin (in green) autoantibodies for children (left) and adults (right). For each subgroup, vertical histograms show the number of patients seropositive for each isotype combination while horizontal histograms show the total number of patients seropositive for each isotype. (C) Proportion of patients with disease onset in childhood or adulthood stratified by autoantibody seropositivity. The size of each pie chart is proportional to the number of individuals captured in that group. Forest plots of the relative risk for adulthood onset given anti-CRB2 or anti-Nephrin seropositivity is plotted below the pie charts. (D) Correlation of uPCR and IgG autoantibody titers in patients with non-biopsied idiopathic nephrotic syndrome (INS, N child = 18), including steroid-sensitive (SSNS, N child = 17) and steroid-resistant (SRNS, N child = 1), or the histological diagnoses of minimal change disease (MCD, N child = 19, N adult = 10) and primary focal segmental glomerulosclerosis (FSGS, N child = 6, N adult = 18). (E) Comparison of uPCR in autoantibody seropositive or seronegative donors shown for the total cohort or for children and adults independently. (F) Representative glomeruli from flash frozen kidney biopsies from the remaining four anti-CRB2 IgG seropositive patients and one seronegative patient present in the quantification in showing CRB2 (green) and IgG (red) co-localization. In D and E, each dot represents a single donor, and summary statistics are shown as median with 95% confidence intervals. P -values were determined using Fisher’s exact tests in C, non-parametric Spearman correlation in D, and Mann-Whitney U -tests in E. This Supplemental Figure is associated with .

    Article Snippet: The standard curve was generated using seven serial dilutions of polyclonal rabbit anti-human CRB2 antibody (custom produced by MediMabs, Montreal, using human CRB2 597- 943 recombinant protein) or monoclonal sheep anti-human Nephrin antibody (RnD systems).

    Techniques: Comparison, MANN-WHITNEY

    (A) Correlation between the frequency of T-bet + CD21 low atypical B cells and serum titers of anti-CRB2 IgG, anti-Nephrin IgG, and their combined titers in children with INS ( N SSNS = 15, N SRNS = 1, N MCD = 7, N FSGS = 3). (B) Correlation between the frequencies of IgD + , IgM + IgD − , and IgM − IgD − plasmablasts (PB) and serum autoantibody titers in children with INS. In all graphs, each dot represents a single donor. A simple linear regression line is shown alongside 95% confidence intervals for ease of visualization. Non-parametric spearman correlations were performed to obtain r and P -values.

    Journal: bioRxiv

    Article Title: Autoantibodies targeting CRB2 and Nephrin correlate with extrafollicular B cells in idiopathic podocytopathies

    doi: 10.1101/2025.09.06.674608

    Figure Lengend Snippet: (A) Correlation between the frequency of T-bet + CD21 low atypical B cells and serum titers of anti-CRB2 IgG, anti-Nephrin IgG, and their combined titers in children with INS ( N SSNS = 15, N SRNS = 1, N MCD = 7, N FSGS = 3). (B) Correlation between the frequencies of IgD + , IgM + IgD − , and IgM − IgD − plasmablasts (PB) and serum autoantibody titers in children with INS. In all graphs, each dot represents a single donor. A simple linear regression line is shown alongside 95% confidence intervals for ease of visualization. Non-parametric spearman correlations were performed to obtain r and P -values.

    Article Snippet: The standard curve was generated using seven serial dilutions of polyclonal rabbit anti-human CRB2 antibody (custom produced by MediMabs, Montreal, using human CRB2 597- 943 recombinant protein) or monoclonal sheep anti-human Nephrin antibody (RnD systems).

    Techniques:

    (A) Correlation between the frequency of T-bet + CD21 low atypical B cells (atBC) and serum titers of anti-CRB2 IgG, anti-Nephrin IgG, and their combined titers in adults with idiopathic podocytopathies ( N MCD = 8, N FSGS =9). (B) Correlation between the frequencies of IgD + , IgM + IgD − , and IgM − IgD − plasmablasts (PB) and serum autoantibody titers in adults with idiopathic podocytopathies. In all graphs, each dot represents a single donor. A simple linear regression line is shown alongside 95% confidence intervals for each of visualization. Non-parametric Spearman correlations were performed to obtain r and P -values. This Supplemental Figure is associated with .

    Journal: bioRxiv

    Article Title: Autoantibodies targeting CRB2 and Nephrin correlate with extrafollicular B cells in idiopathic podocytopathies

    doi: 10.1101/2025.09.06.674608

    Figure Lengend Snippet: (A) Correlation between the frequency of T-bet + CD21 low atypical B cells (atBC) and serum titers of anti-CRB2 IgG, anti-Nephrin IgG, and their combined titers in adults with idiopathic podocytopathies ( N MCD = 8, N FSGS =9). (B) Correlation between the frequencies of IgD + , IgM + IgD − , and IgM − IgD − plasmablasts (PB) and serum autoantibody titers in adults with idiopathic podocytopathies. In all graphs, each dot represents a single donor. A simple linear regression line is shown alongside 95% confidence intervals for each of visualization. Non-parametric Spearman correlations were performed to obtain r and P -values. This Supplemental Figure is associated with .

    Article Snippet: The standard curve was generated using seven serial dilutions of polyclonal rabbit anti-human CRB2 antibody (custom produced by MediMabs, Montreal, using human CRB2 597- 943 recombinant protein) or monoclonal sheep anti-human Nephrin antibody (RnD systems).

    Techniques: