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Circulating DC subsets in traumatised patients 1–240 h after injury. (a, b) Time course of the percentage of <t>CD11c</t> + CD123 − cDCs and CD11c − CD123 + pDCs among CD45 + leukocytes (set at 100%) in (a) volunteers and all patients, and (b) in both patient groups after traumatic injury. Comparison between groups and between consecutive time points in one group (only significant changes related to the previous time point are shown): mixed‐effect model, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. (c) Correlation of the percentage of cDCs and pDCs to clinical parameters. In the correlation matrix, square colour indicates the magnitude of correlation; only significant correlations (Spearman) are shown.
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Circulating DC subsets in traumatised patients 1–240 h after injury. (a, b) Time course of the percentage of <t>CD11c</t> + CD123 − cDCs and CD11c − CD123 + pDCs among CD45 + leukocytes (set at 100%) in (a) volunteers and all patients, and (b) in both patient groups after traumatic injury. Comparison between groups and between consecutive time points in one group (only significant changes related to the previous time point are shown): mixed‐effect model, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. (c) Correlation of the percentage of cDCs and pDCs to clinical parameters. In the correlation matrix, square colour indicates the magnitude of correlation; only significant correlations (Spearman) are shown.
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Circulating DC subsets in traumatised patients 1–240 h after injury. (a, b) Time course of the percentage of <t>CD11c</t> + CD123 − cDCs and CD11c − CD123 + pDCs among CD45 + leukocytes (set at 100%) in (a) volunteers and all patients, and (b) in both patient groups after traumatic injury. Comparison between groups and between consecutive time points in one group (only significant changes related to the previous time point are shown): mixed‐effect model, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. (c) Correlation of the percentage of cDCs and pDCs to clinical parameters. In the correlation matrix, square colour indicates the magnitude of correlation; only significant correlations (Spearman) are shown.
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Circulating DC subsets in traumatised patients 1–240 h after injury. (a, b) Time course of the percentage of <t>CD11c</t> + CD123 − cDCs and CD11c − CD123 + pDCs among CD45 + leukocytes (set at 100%) in (a) volunteers and all patients, and (b) in both patient groups after traumatic injury. Comparison between groups and between consecutive time points in one group (only significant changes related to the previous time point are shown): mixed‐effect model, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. (c) Correlation of the percentage of cDCs and pDCs to clinical parameters. In the correlation matrix, square colour indicates the magnitude of correlation; only significant correlations (Spearman) are shown.
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Circulating DC subsets in traumatised patients 1–240 h after injury. (a, b) Time course of the percentage of <t>CD11c</t> + CD123 − cDCs and CD11c − CD123 + pDCs among CD45 + leukocytes (set at 100%) in (a) volunteers and all patients, and (b) in both patient groups after traumatic injury. Comparison between groups and between consecutive time points in one group (only significant changes related to the previous time point are shown): mixed‐effect model, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. (c) Correlation of the percentage of cDCs and pDCs to clinical parameters. In the correlation matrix, square colour indicates the magnitude of correlation; only significant correlations (Spearman) are shown.
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Circulating DC subsets in traumatised patients 1–240 h after injury. (a, b) Time course of the percentage of CD11c + CD123 − cDCs and CD11c − CD123 + pDCs among CD45 + leukocytes (set at 100%) in (a) volunteers and all patients, and (b) in both patient groups after traumatic injury. Comparison between groups and between consecutive time points in one group (only significant changes related to the previous time point are shown): mixed‐effect model, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. (c) Correlation of the percentage of cDCs and pDCs to clinical parameters. In the correlation matrix, square colour indicates the magnitude of correlation; only significant correlations (Spearman) are shown.

Journal: Clinical & Translational Immunology

Article Title: Long‐lasting changes in circulating dendritic cell and monocyte subsets, and altered expression of EMR2, CD97 and EMR3 on these cells in the posttraumatic course

doi: 10.1002/cti2.70040

Figure Lengend Snippet: Circulating DC subsets in traumatised patients 1–240 h after injury. (a, b) Time course of the percentage of CD11c + CD123 − cDCs and CD11c − CD123 + pDCs among CD45 + leukocytes (set at 100%) in (a) volunteers and all patients, and (b) in both patient groups after traumatic injury. Comparison between groups and between consecutive time points in one group (only significant changes related to the previous time point are shown): mixed‐effect model, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. (c) Correlation of the percentage of cDCs and pDCs to clinical parameters. In the correlation matrix, square colour indicates the magnitude of correlation; only significant correlations (Spearman) are shown.

Article Snippet: CD11c PE‐Cy7 , B‐Ly6 , Becton Dickinson GmbH (BD, Heidelberg, Germany), 561 356.

Techniques: Comparison

Characterisation of circulating monocyte and DC subsets for EMR2, CD97, and EMR3 expression in flow cytometry. (a, b) Analysis of EMR2, EMR3, and CD97 in (a) monocytes (CD14 hi CD16 − classical, CD14 hi CD16 + intermediate, CD14 lo CD16 + non‐classical) and (b) DC subsets (CD11c + CD123 − conventional, CD11c − CD123 + plasmacytoid); DCs are EMR3‐negative. Left: The main gating strategy is shown in single steps. The percentage of cells within a figure is set to 100%, and the percentage of gated cells, further examined, is indicated. Right: Median fluorescence intensity (MFI; right‐upper corner) of isotype control‐on and adhesion GPCR antibody‐stained cells; the percentages of positive cells are indicated at the gate. Exemplary data of an injured patient (ISS 32) 24 h after trauma are shown.

Journal: Clinical & Translational Immunology

Article Title: Long‐lasting changes in circulating dendritic cell and monocyte subsets, and altered expression of EMR2, CD97 and EMR3 on these cells in the posttraumatic course

doi: 10.1002/cti2.70040

Figure Lengend Snippet: Characterisation of circulating monocyte and DC subsets for EMR2, CD97, and EMR3 expression in flow cytometry. (a, b) Analysis of EMR2, EMR3, and CD97 in (a) monocytes (CD14 hi CD16 − classical, CD14 hi CD16 + intermediate, CD14 lo CD16 + non‐classical) and (b) DC subsets (CD11c + CD123 − conventional, CD11c − CD123 + plasmacytoid); DCs are EMR3‐negative. Left: The main gating strategy is shown in single steps. The percentage of cells within a figure is set to 100%, and the percentage of gated cells, further examined, is indicated. Right: Median fluorescence intensity (MFI; right‐upper corner) of isotype control‐on and adhesion GPCR antibody‐stained cells; the percentages of positive cells are indicated at the gate. Exemplary data of an injured patient (ISS 32) 24 h after trauma are shown.

Article Snippet: CD11c PE‐Cy7 , B‐Ly6 , Becton Dickinson GmbH (BD, Heidelberg, Germany), 561 356.

Techniques: Expressing, Flow Cytometry, Fluorescence, Control, Staining