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Becton Dickinson pe anti-igd
Plasmodium berghei ANKA infection induces IgM+ memory B cells. C57BL/6 mice were infected with P. berghei ANKA and treated with anti-malarial drugs from day 5 pi. (A) Gating strategy used to identify IgM+ memory B cells by flow cytometry, depicting gated <t>IgD−CD19+</t> B cells that were negative <t>for</t> <t>CD21</t> and CD138 to exclude marginal zone B cells and plasma cells, respectively. Memory B cells were then identified by high expression of CD38 and low levels of Fas, to exclude GC B cells. IgM+ memory B cells were identified among this compartment. (B) Absolute number of IgM+ memory B cells in P. berghei ANKA-infected mice on day 24 pi and naive controls. Error bars represent the mean of 8–10 mice ± s.e.m., ***P < 0.005.
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Plasmodium berghei ANKA infection induces IgM+ memory B cells. C57BL/6 mice were infected with P. berghei ANKA and treated with anti-malarial drugs from day 5 pi. (A) Gating strategy used to identify IgM+ memory B cells by flow cytometry, depicting gated <t>IgD−CD19+</t> B cells that were negative <t>for</t> <t>CD21</t> and CD138 to exclude marginal zone B cells and plasma cells, respectively. Memory B cells were then identified by high expression of CD38 and low levels of Fas, to exclude GC B cells. IgM+ memory B cells were identified among this compartment. (B) Absolute number of IgM+ memory B cells in P. berghei ANKA-infected mice on day 24 pi and naive controls. Error bars represent the mean of 8–10 mice ± s.e.m., ***P < 0.005.
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Plasmodium berghei ANKA infection induces IgM+ memory B cells. C57BL/6 mice were infected with P. berghei ANKA and treated with anti-malarial drugs from day 5 pi. (A) Gating strategy used to identify IgM+ memory B cells by flow cytometry, depicting gated <t>IgD−CD19+</t> B cells that were negative <t>for</t> <t>CD21</t> and CD138 to exclude marginal zone B cells and plasma cells, respectively. Memory B cells were then identified by high expression of CD38 and low levels of Fas, to exclude GC B cells. IgM+ memory B cells were identified among this compartment. (B) Absolute number of IgM+ memory B cells in P. berghei ANKA-infected mice on day 24 pi and naive controls. Error bars represent the mean of 8–10 mice ± s.e.m., ***P < 0.005.
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Becton Dickinson anti-igd pe iag2
Immunologic findings in CVID patients and control groups (* P <0.05).
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Becton Dickinson anti-human igd (ia6-2
Immunologic findings in CVID patients and control groups (* P <0.05).
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Image Search Results


Plasmodium berghei ANKA infection induces IgM+ memory B cells. C57BL/6 mice were infected with P. berghei ANKA and treated with anti-malarial drugs from day 5 pi. (A) Gating strategy used to identify IgM+ memory B cells by flow cytometry, depicting gated IgD−CD19+ B cells that were negative for CD21 and CD138 to exclude marginal zone B cells and plasma cells, respectively. Memory B cells were then identified by high expression of CD38 and low levels of Fas, to exclude GC B cells. IgM+ memory B cells were identified among this compartment. (B) Absolute number of IgM+ memory B cells in P. berghei ANKA-infected mice on day 24 pi and naive controls. Error bars represent the mean of 8–10 mice ± s.e.m., ***P < 0.005.

Journal: Parasitology

Article Title: IgM + memory B cells induced in response to Plasmodium berghei adopt a germinal centre B cell phenotype during secondary infection

doi: 10.1017/S003118202000061X

Figure Lengend Snippet: Plasmodium berghei ANKA infection induces IgM+ memory B cells. C57BL/6 mice were infected with P. berghei ANKA and treated with anti-malarial drugs from day 5 pi. (A) Gating strategy used to identify IgM+ memory B cells by flow cytometry, depicting gated IgD−CD19+ B cells that were negative for CD21 and CD138 to exclude marginal zone B cells and plasma cells, respectively. Memory B cells were then identified by high expression of CD38 and low levels of Fas, to exclude GC B cells. IgM+ memory B cells were identified among this compartment. (B) Absolute number of IgM+ memory B cells in P. berghei ANKA-infected mice on day 24 pi and naive controls. Error bars represent the mean of 8–10 mice ± s.e.m., ***P < 0.005.

Article Snippet: To detect of IgM + memory B cells, splenocytes were stained with: APC anti-CD21 (7G6, Miltenyi Biotec), FITC anti-IgM (Il/41, BD Biosciences), PE anti-IgD (11–26c.2a, BD Biosciences), PerCP Cy5.5 anti-CD19 (1D3, BD Biosciences), BV650 anti-Fas/CD95 (Jo2, BD Biosciences), PE/Cy7 anti-CD38 (90, BioLegend) and BV421 anti-CD138 (281–2, BioLegend).

Techniques: Infection, Flow Cytometry, Expressing

Immunologic findings in CVID patients and control groups (* P <0.05).

Journal: International Journal of Immunopathology and Pharmacology

Article Title: CD4 + CD25 + Foxp3 + T regulatory cells, Th1 (CCR5, IL-2, IFN-γ) and Th2 (CCR4, IL-4, Il-13) type chemokine receptors and intracellular cytokines in children with common variable immunodeficiency

doi: 10.1177/0394632015617064

Figure Lengend Snippet: Immunologic findings in CVID patients and control groups (* P <0.05).

Article Snippet: CD3/CD4/CD8/CD45, CD3/CD19/CD16/56/CD45, CD3/HLA DR multicolor antibody reagents, and anti-CD27 FITC (clone M-T271), anti-IgD PE (clone IAG2), and anti-IgM PE (clone G20-127) were all purchased from BD Biosciences.

Techniques: